/OJ11V3-JO vlOS -ANGELA -OF-CALIFO% $$[. ,^' ^/ > . ^\V\E-l'MVtRV^ A U r^ , ^^^ ^LiBRARY^ >0Aavaan^ ^ONVSOI^ SYNOPSIS OF LECTURES UPON Diseases of the Nervous System BY PROF. M. ALLEN STARR COLLEGE OF PHYSICIANS AND SURGEONS MEDICAL DEPARTMENT OF COLUMBIA COLLEGE NEW YORK TROW DIRECTORY, PRINTING AND BOOKBINDING CO. 201-213 EAST TWELFTH STREET 1894 COPYRIGHT, 1893, BY M. ALLEN STARR WL loo SYNOPSIS OF LECTURES UPON DISEASES OF THE NERVOUS SYSTEM. A KNOWLEDGE of the structure and functions of the central nervous system is an essential preliminary to the study of its dis- eases. The human nervous system is the most complex of all nervous structures, and is the culmination of the process of evo- lution It will aid in the understanding of its structure if the various stages in its evolution are known. THE EVOLUTION OF THE NERVOUS SYSTEM. The simplest form of a nervous system consists of a single mass of gray matter with a sensory and a motor nerve. The mass of gray matter receives impulses sent from the sur- face by the sensory fibre, acts in response to the impulse, and the action is transmitted to a motor mechanism by the motor nerve. Example. The closure of an oyster-shell when the oyster feels any object touching its sensory surface. Parallel action in hu- man system any spinal reflex e.g., knee-jerk. Several such single masses may be joined to one another, each with its sensory and motor nerve. The masses receive im- pulses in succession and act in succession. Example. Wave-like motion of a jelly-fish or caterpillar. A compound type of nervous system consists of several sub- ordinate masses joined together and presided over by a single higher mass, which is joined to each of the lower masses. The higher mass receives impulses from the lower masses, not di- rectly from the surface. It sends impulses to the motor mech- anisms through the lower masses, not directly. It secures a cer- 4 DISEASES OF THE NERVOUS SYSTEM. tain definite succession and combination of action in the lower masses. Examples. The nervous system of a frog experimentally de- prived of its hemispheres, capable of automatic acts of swim- ming. The automatic act of respiration in man. In man the facial, laryngeal, intercostal, thoracic, and diaphragmatic respira- tory muscles act in definite succession and rhythm in the act of breathing ; and this act is presided over by a single centre in the medulla controlling the lower medullary and spinal centres. The highest type of nervous system is the complex type. There are the lower centres as in the simple type. There are higher centres controlling the lower centres, as in the compound type. There is a supreme mass controlling both the others. This is the form found in all vertebrates, and the degree of evolution in the highest or supreme mass determines the place of the animal in the scale of intelligence. In man the supreme mass is the cerebral cortex, the next lower or automatic centres are the optic thalami and basal gan- glia, including gray masses in the cerebral ax*is ; the lowest or reflex centres are the cranial nerve nuclei in the cerebral axis and the gray matter of the spinal cord segments. These distant gray masses are joined with one another in all possible combinations by means of the \vhite nerve tracts, which pass in all directions around and within them. Read Herbert Spencer, " Principles of Psychology," Part I., Chaps. I. -IV. Charles Mercier, "The Nervous System and the Mind," Part I. THE HUMAN NERVOUS SYSTEM. The human nervous system consists of a peripheral system and a central system. The peripheral system comprises all the nerves. The central system includes : First. The spinal cord and cranial nerve nuclei. Secondly. The cerebellum ; gray masses of the medulla, pons, and crura cerebri ; corpora quadrigemina, optic thalami, and cor- pora striata. Thirdly. The cerebral cortex. DISEASES OF THE NERVOUS SYSTEM. THE PERIPHERAL NERVES AND THEIR DISEASES. STRUCTURE of the nerves. Bundles of nerve fibres large or small. Structure of a nerve fibre : i. Axis cylinder, a long process of some nerve cell. 2. Medullary sheath of myelin a fatty in- sulator, interrupted at the nodes of Ranvier. 3. Connective tissue sheath of Schwann, with its nucleus. Nerve fibres are bound into bundles by connective tissue ; endoneurium, peri- neurium. The visceral nerve fibres have no medullary sheath. All nerve fibres branch during their course in the central nervous system, sending out "collaterals," but do not branch in their peripheral course. They arise from a nerve cell. They terminate in fine brush-like expansions which are spread out in the skin, or on a muscle, or around another nerve cell. Nerves are divided into motor nerves and sensory nerves, ac- cording to the mechanism to which they are attached. Motor nerves convey impulses outward, sensory inward. Motor nerves grow outward from large nerve cells in the spinal cord. Sen- sory nerves grow from cells in the posterior spinal ganglia, which send one branch to the surface, and the other into the spinal cord. NEURITIS. Neuritis may occur in a single nerve, or in a plexus. Causes. Injuries, strains, pressure, compression in fractures, rheumatism, gout, cold. Pathology. i. Parenchymatous neuritis, congestion and exu- dation in nerve- trunk ; swelling and degeneration of individual fibres ; i, axis cylinder broken and disintegrated in fatty mass ; 2, medullary substance separated into segments and fatty globules, and mingled with granules and nucleated cells ; 3, connective tissue sheath shrunken and empty. Nuclei multiply. Products of degeneration liquefy and are absorbed. 6 DISEASES OF THE NERVOUS SYSTEM. Regeneration occurs by growth of new fibres outward from the healthy stump into the old sheath. 2. Interstitial neuritis. The connective tissue of the endo- neurium and perineurium increases in volume and the nerve- fibres are compressed by the congested vessels and by the new tissue. These forms usually occur together in non-traumatic cases. Symptoms. Weakness or paralysis with atrophy and reaction of degeneration in muscles supplied by nerves involved. Reaction of degeneration (R. D.) is a change in the action of the nerves and muscles to the electric currents. The response of the nerve to both currents is lost. The muscle loses its faradic reaction. The galvanic reaction is changed, the muscle responding more actively to the closure of the positive pole (anode) than to that of the negative pole (kathode). Numbness or anaesthesia in skin sup- plied by nerve involved. Vasomotor and trophic changes in the distribution of nerve involved. Coldness from sluggish meta- bolism ; glossy skin; oedema ; pain and tenderness at seat of in- flammation in interstitial cases. Course. Slow spontaneous recovery when continuity of nerve is preserved. Otherwise, no recovery. Treatment. If nerve is broken unite divided ends. Rest the part injured but exercise the muscles paralyzed by electricity and massage. Use hot applications, sedative lotions. Protect from cold by cotton batting. Morphine for pain. MULTIPLE NEURITIS. Multiple neuritis is an inflammatory or degenerative disease of the peripheral nervous system varying in extent and inten- sity and affecting symmetrical parts of the body. The motor nerves may be involved alone (e.g., in lead and mercury poisoning), or the sensory nerves alone (e.g., in coal-gas poisoning), or both .may be involved together (e.g., in alcoholic neuritis). The distal parts of the nerves are commonly affected to a greater extent than the central parts. Hence the symptoms appear chiefly in the distal parts of the extremities. The pathological process is the same as in simple neuritis and may be parenchymatous alone, or interstitial alone, or both. Etiology. i. Toxic cases : Alcohol, lead, arsenic, bisulphide of carbon, copper, zinc, mercury, phosphorus, coal gas. DISEASES OF THE NERVOUS SYSTEM. 7 2. Infectious cases : Diphtheria, typhoid, scarlet fever, measles, malaria, leprosy, beri beri, grippe. 3. Rheumatic cases : Exposure to cold, over-exertion. 4. Secondary to anaemia, tuberculosis, syphilis, septicaemia, general malnutrition, and diabetes. Symptoms. Acute or sub-acute onset with fever, io3-io4 F., and general febrile symptoms sometimes without fever. Sensory Symptoms. First to occur. Pain Sharp, severe, lo- cated in limbs, increased by motion or pressure ; muscular and nerve tenderness, sensitiveness. Paraesthesiae Burning, tingling, numbness, band about legs and body. Anaesthesia In tips of fingers and toes, extends up limbs. Ataxia In fine movements and loss of sense of position. Motor Symptoms. Paralysis. In extensors, dropped wrist and foot, general inability to walk or move in bed ; contractures ; cranial nerves may be paralyzed causing symptoms in face. Atrophy Rapid in onset. R. D., or diminution in electric contractility ; loss of deep reflexes ; no paralysis of sphincters. Trophic Symptoms. Vasomotor paralysis ; glossy skin ; oedema ; abnormal growth of nails and hair ; sweating profuse ; no bed- sores ; urticaria. Certain cases present peculiar features in their course. 1. Alcoholic Neuritis. (a) Rapid onset is the rule, with delirium and delusions, subsequently imperfect memory of recent events. Total paralysis, with very great pain ; anaesthesia very marked, also tremor and tenderness ; dropped wrists and feet ; or (b) All symptoms of locomotor ataxia develop rapidly, except bladder and rectal loss of control. In both forms there is danger of heart failure or death from exhaustion, due to complicating gastritis. Usually there is, rapid increase of symptoms for three or four weeks, and then, after a stationary period of two months, a slow progress to recovery, the duration being from six to twelve months. 2. Lead Neuritis. Onset with intestinal colic, lead line on gums. Paralysis without sensory disturbance in hands, causing dropped wrists. May affect all muscles of arms and legs, and go on to sensory symptoms with delusions, but this is rare. Gradual recovery, when poison is eliminated, in four months. 3. Arsenical Cases. Gastric disturbance at outset. Then paralysis with ataxia, tremor, atrophy, and great numbness, but 8 DISEASES OF THE NERVOUS SYSTEM. little pain ; legs and arms equally affected. Recovery in two to six months, depending on original severity. 4. Coal Gas Cases. Subacute and slight, chiefly sensory, numbness for a long time in fingers, hands, and feet. 5. Diphtheritic Cases. Severe paralysis of all extremities, usually without sensory disturbance, cranial nerves frequently affected. It begins in uvula, and swallowing and talking become difficult. Eyes are often turned. Ataxia is marked in some cases. Never pain. Progress to recovery usual in three months. 6. Epidemic Form. (Beri beri.) Occurs in Brazil, Red Sea, India, Borneo. Japan. Several types : acute pernicious, chronic cedematous, chronic atrophic. Too rare to need attention here. (See Gowers, L, 151 ; also New York Medical Record, February 12, 1887.) Diagnosis. From anterior poliomyelitis : by pain, tenderness along nerves, sensory symptoms, distribution of paralysis sym- metrically. From locomotor ataxia : by rapid onset and paralysis, preservation of control of bladder, and absence of Argyle Robertson pupil. From myelitis : by absence of affec- tion of bladder and rectum, by absence of bed-sores, and tender- ness of spine to heat, and by distribution of symptoms in periph- ery. Prognosis. Good in large majority of cases; slow recovery ; bad when heart becomes rapid and respiration poor. Treatment. Rest in bed. Warm applications by packs to limbs. Rubbing with oil ; gentle massage if possible. Prevent deformities and contractures by proper position of limbs. Elec- tricity, galvanism through nerves and to muscles after acute stage. Baths, warm, 98 F., for half hour several times daily. Attention to diet, nourish well, cut off alcohol in all cases. General and nerve tonics ; iron, quinine, strychnine. In acute stage, sodium salicylate, gr. x., q. 3 hr., and seda- tives, morphine, phenacetine. In chronic stage, arsenic -fa gr. t.i.d., cod liver oil. DISEASES OF THE NERVOUS SYSTEM. THE SPINAL CORD AND CRANIAL NERVE NUCLEI. THE spinal cord in man is made up of thirty-one segments each of which consists of a mass of gray matter joined to a pair of spinal nerves. There is no apparent line of boundary between adjacent segments, the cord being a long cylindrical organ. But in snakes and rabbits the area of gray matter is much larger opposite the entrance of nerves than between them, and in fishes there is a visible boundary between adjacent segments. Each segment presents a symmetrical arrangement of its two halves. Each half consists of a central collection of gray matter surrounded by white tracts. Each gray mass has an an- terior horn, a central mass, and a posterior horn. To each horn nerve fibres are joined making the anterior and posterior nerve roots. The two halves are separated from one another in front by the anterior fissure, and behind by the posterior septum. They are joined together by the anterior white commissure and by the gray commissure in which lies the central canal of the cord. The functions of each segment are shown in the table on page 10. THE ANTERIOR HORNS OF THE SPINAL CORD. These vary greatly in size and shape in various segments, being large opposite the entrance of the cervical and lumbo- sacral nerves and thus causing the cervical and lumbo-sacral enlargements of the cord. , Their size and shape depend upon the number of groups of cells found at different levels ; for the horns are made up of cells large, polygonal cells with nucleus and nucleolus collected into distinct groups. Some groups of cells lie on the edge of the horn, making projections of the gray mass into the white columns. These groups are found in all the higher vertebrates and are not pecul- iar to man. Other groups lie within the horn and these are 10 DISEASES OF THE NERVOUS SYSTEM. Segment. Muscles. Reflex. Sensation. zd and 3d Cer- Sterno mastoii Tra- Hypochondrmm (?) Back of head to vertex. vical. pezius. Sudden inspiration produced Neck. Scaleni and neck. by sudden pressure beneath Diaphragm. the lower border of ribs. 4th Cervical. Diaphragm. Pupil 4-7 cervical. Neck. Deltoid. Dilatation of the pupil pro- ' Upper shoulder. Biceps. Coraco-brachialis duced by irritation of neck. Outer arm. Supinator Longus. Rhomboid. Supra & infra spinatus. 5th Cervical. Deltoid. Scapular. Back of shoulder and arm. Biceps Coraco-brachialis 5th Cervical to ist Dorsal. Outer side of arm and fore- Brachialis anticus. Irritation of skin over thescap- arm. Supinator longus. ula produces contraction of Anterior upper two-thirds Supinator brevis. the scapular muscles. of arm. Deep muscles of shoul- der blade. Supinator Longus. Rhomboid. Teres minor.! Tapping its tendon in wrist pro- Pectoralis (clav. part). duces flexion of forearm. Serratus magnus. 6th Cervical. Brach. anticus. Triceps. Outer side of arm and fore- Pectoralis (clav. part). 5th to 6th Cervical. arm. Serratus magnus. Tapping elbow tendon produ- Inside and front of fore- Triceps. ces extension of forearm. arm. Extensors of wrist and fingers. Posterior wrist. Pronators. 6th to Sth Cervical. Tapping teudons causes ex- tension of hand. 7th Cervical. Triceps (long head). Inner and back of arm and Extensors of wrist and forearm. fingers. Anterior wrist. Pronators of wrist. 7th-8th Cervical. Radial distribution in the Flexors of wrist. Tapping anterior tendon causes hand. Subscapular. flexion of wrist. Pectoralis (costal part). Palmar. ?th Cerv.- ist Dorsal. Latissimus dorsi. Stroking palm causes closure Teres major. of fingers. 8th Cervical. Flexors of wrist and Forearm and hand: median fingers. and ulnar areas. Intrisic muscles of hand. ist Dorsal. Extensors of thumb. Ulnar distribution to hand. Intrinsic hand muscles. Thenar and hypothenar eminences. zd and izth Muscles of back and ab- Epigastric. 4th-7th Dorsal. Skin of chest and abdomen, Dorsal. domen. Erectores spins. in bands running around Tickl'g mammary region causes and downward corre- retraction of the epigastrium. spending to spinal nerves. Abdominal, 7th- nth Dorsal. Stroking side of abdomen caus- Upper eluteal region. es retraction of belly. ist Lumbar. Ilio-psoas. Cremasteric. ist~3d Lumbar. Skin over groin and front Sartorius. Stroking inner thigh causes of scrotum, and narrow retraction of scrotum. band down front of the zd Lumbar. Ilio-psoas. Sartorius. Patella tendon. thigh and leg. Inner side of thigh. Flexors of knee( Remak). Quadriceps femoris. Striking tendon causes exten- sion of leg. 2d-4th Lumbar. Outer side of thigh. 3d Lumbar. Quadriceps femoris. Inner rotators of thigh. Abductors of thigh. Inner side of thigh and leg to ankle. 4th Lumbar. Abductors of thigh. Gluteal. Inner side of foot. Adductors of thigh. 4th-5th Lumbar. Flexors of knee (Kerrier), Tibialis anticus. Stroking buttock causes dimpl- ing in fold of buttock. 5th Lumbar. Outward rotators of thigh. Achilles tendon. Over extension causes rapid Lower gluteal region back of thigh. Leg and foot Flexors of knee (Ferrier). Flexors of ankle. Peronei. flexion of ankle, called ankle clonus. outer part. Extensors of toes. tst and id Flexors of ankle. Plantar. Leg and foot except inner Sacral. I-ong flexor of toes. Intnnsic muscles of foot. Tickling sole of foot causes flexion of toes and retraction side. of leg. 3d to sth Sao Peroneus longus. Bladder and rectal centre. Perineum and back of scro- ral. | > turn. Anus. DISEASES OF THE NERVOUS SYSTEM. II peculiar to man and the higher apes. Each group of cells pre- sides over the action of a muscle and maintains its tone and nutrition, so that all motor impulses to the muscle, whether reflex, automatic, or voluntary, proceed from the group of cells. The outer groups govern muscles of flexion, extension, pronation and supination of the larger joints. The inner groups govern the small muscles of the fingers and toes. Hence the outer groups are said to preside over fundamental motions and the inner groups over accessory motions. The thumbless monkey has no inner groups in the cervical region. These are present in monkeys with thumbs and in man. When the inner groups are Destroyed by disease, the finger mo- tions are paralyzed. In each segment there may be from two to eight groups of cells. Any group may extend through several segments. If a single segment is destroyed by disease several muscles will be paralyzed. But no muscle will be totally paralyzed unless its entire group of cells is destroyed. Total paralysis with complete atrophy in a muscle indicates destruction of the entire group of cells which govern the muscle. If the group extends through several segments the paralysis implies disease in all the seg- ments. The table shows the situation in the various segments of the groups of cells governing the various muscles, so far as these have been determined. ANTERIOR POLIOMYELITIS. Anterior Poliomyelitis is a disease limited to the anterior horns of the spinal cord. It may be acute or chronic. Acute anterior poliomyelitis is a common disease of childhood known as infantile paralysis. It occasionally occurs in adults. Chronic anterior poliomyelitis is an uncommon disease of adult life or old age, known as atrophic paralysis. Acute Anterior Poliomyelitis. Etiology. Occurs chiefly between two to five years, when exertion is greatest, in the summer, May to September, when exposure is greatest to heat, occasion- ally after falls and after fevers ; it is probably an acute infectious disease in many cases. Pathology. Lesion is an acute inflammation of the entire gray matter of the anterior horn, the cells and interlacing fibres being affected. The cells become swollen, undergo degeneration, and liquefy, and then shrivel and atrophy. The fibres are separated 12 DISEASES OF THE NERVOUS SYSTEM. from their cells and atrophy. The neuroglia is infiltrated with inflammatory corpuscles. The capillaries are distended and fre- quently rupture. The process may go on to complete destruc- tion of the cells or may be arrested at any stage. If it is arrested early, repair may ensue and the cells regain their former appearance. If it goes on the result is a diminution in the size of the horn, a change in its shape and a contraction of the entire cord at the level of the lesion. As a rule the entire anterior horn is at first involved, but the permanent destruction is limited to one or two groups of cells on one side only. In as much as each motor nerve^bre comes from and is a part of the motor cell the nerve fibres degenerate when the motor cells are destroyed. Atrophy of the motor nerve-roots and motor- nerves from the anterior horns to the muscles is therefore part of the lesion in anterior poliomyelitis. The deformity of the spinal cord at the level of the lesion, and the atrophy of the nerve trunks are due in part to these changes in the nerve fibres. The muscles which are paralyzed atrophy rapidly, and when recovery does not occur they remain small. Mije no special groups of cells are known to control the 3 3n-of the bones, it is found that if the gray matter near the central region of the segment is destroyed by the diseas,e, the bones are much retarded in their growth. Hence in a severe case of infantile palsy the limb affected is smaller than other limbs in all its parts. But trophic changes in the skin, such as sores, glossy skin, or gangrene, do not occur. Through the an- terior horns pass fibres from the central region which control the vascular tone and metabolic processes. Hence in lesions of the anterior horn symptoms due to the destruction of these fibres ensue, viz., sluggish circulation, cyanosis, and lowered tem- perature, with imperfect nutrition. Symptoms. Sudden onset with fever 100 to 103 F., occa- sionally without. Febrile symptoms : Headache, loss of appetite, nausea, vomiting, diarrhoea. Restlessness : often convulsions and delirium. The fever rarely continues more than two tp three days. Occasionally pain in the back and limbs is complained of when child is old enough to talk. Paralysis appears suddenly. Sometimes is found in the* morn- ing ; is complete and extensive either in one limb or more ; legs oftener than arms, 4 to i ; one limb more than the other. Maxi- DISEASES OF THE NERVOUS SYSTEM. 13 mum is reached in first week. Remains stationary for two to six weeks and then improves. Result is recovery, which is partial ; some muscles remain paralyzed. The affected limb atrophies rapidlv. Atrophy is most intense in the muscles permanently weak. There is a change in the electric reactions in the paralyzed muscle. R. D. Loss of faradic excitement in two weeks or sooner. Increase at first, then decrease, in galvanic excitability. Muscles contract slowly instead of quickly, more forcibly to the positive than to the negative pole. The nutrition of the entire limb suffers ; bones small and growth impaired ; fat is less frrm, ano> skin is cold ; but no bed- sores appear. The sphincters are not affected. The reflex action is lost at the level affected, not changed elsewhere. Course. There is a progressive improvement which begins within two months, but usually some muscles remain paralyzed and atrophied, and the joints moved by these may become de- formed ; spine curved. The muscles most frequently affected are : The peronei and tibialis anticus in the leg, hence talipes equinus and varus ; the muscles of the calf, and anterior part of the thigh ; the deltoid, biceps, supinators, and spinati in the arm, hence subluxation of humerus ; the muscles of the hand and fore- arm. General health is unaffected. / In adults acute anterior poliomyelitis presents the same symp- toms, but fever is less severe and pain is greater in muscles. Extent of initial paralysis is greater. ^Occasionally the onset is slow so that case is called subacute, developing in two to four weeks progressively, remaining 10r^ri;ime stationary and then subsiding?* Diagnosis. From acute rheumatism in infants. Rheumatism may produce immobility of joints. It also causes pain, redness, swelling of joints, and tenderness. Prognosis. Good as to life. As to recovery, at end iff two weeks test faradic reaction. The muscles in' which it persists will recover entirely. At end of three months test again. The muscles in which it has returned wilj recover partially. At end of six months test again. The muscles which do not re- spond will never recover. As to use of lin>b it depends on growth of bone ; e.g., short leg on developn^nt of deformity and 'contractures ; e.g., talipes. -. 14 DISEASES OF THE NERVOUS SYSTEM. Treatment. In acute stage : Cup or blister the spine and keep quiet. Give ergot and bromide, and antipyretics. In chronic stage : Rubbing, warm clothing, galvanism to the muscles, interrupted, continuous. Strychnine T ^ to -^ t.i.d., ac- cording to age. Prevent or remedy deformities by apparatus or surgical operation. Chronic Anterior Poliomyelitis. Progressive muscular atrophy occurs in adults between thirty and fifty years ; is a rare disease. Etiology. Falls and injuries, exposure to damp and cold, alco- holic and sexual excesses, lead poison ing (?). Symptoms. Gradually increasing atrophic paralysis, several months in onset, preceded by fatigue and weakness and loss of weight. Muscles become flabby, then atrophied and paralyzed. It begins in legs and extends upward (peroneal type). It may begin in hands and then extend to shoulders and in- vade the back (Aran Duchenne type). Finally, all the muscles of the body, including face and tongue, may be affected. The tendon reflexes are lost. There are fibrillary twitchings in muscles. There are electrical changes which vary in different cases, usually R. D. is found. The circulation is poor in the limb, skin cold and blue. There is no sensory disturbance except slight numbness. There are no visceral symptoms, no disturbance of bladder and rectal control. Bedsores do not develop. Course. Gradual increase after a long period of stationary state. Sometimes a steady progress to bulbar paralysis and death. Treatment. Similar to chronic stage of acute anterior polio- myelitis. CRANIAL NERVE NUCLEI. The groups of cells in the cerebral axis (medulla oblongata, pons varolii," and crura cerebri) which give origin to the motor cranial nerves lie partly on the floor of the fourth ventricle (XII., VI., IV., III.), and partly deep beneath the floor in the formatio reticularis (XL, IX., VII., Vm.). These groups of cells are quite homologous to the groups in the anterior horns of the cord, and are subject to diseases whose pathology is the same of that of poliomyelitis. DISEASES OF THE NERVOUS SYSTEM. 1 5 BULBAR PARALYSIS OR GLOSSO-LABIO-LARYNGEAL PARALYSIS (Rare). Symptoms. Slowly progressing paralysis with atrophy in the motor cranial nerve nuclei muscles. 1. Disturbance of speech. Alalia, tongue letters, R L D T, due to paralysis of XII. nerve nucleus. Atrophy and tremor of tongue with paralysis. Chewing, swallowing impaired. 2. Muscles of lips and face become weak and thin, due to paralysis of VII. nerve nucleus. Alalia extends to lip letters, P B V F. Atrophy and tremor of lips with paralysis. Whistling, facial expression impaired. Saliva runs and is increased. 3. Muscles of pharynx and larynx affected, due to paralysis of the IX. and XI. nerve nuclei. Food regurgitates or cannot be swallowed ; reflex action impaired ; larynx unprotected ; voice monotonous, low ; cough impossible. There is no change of sensation or of taste. Pulse sometimes rapid, 100 to 130. Duration two to five years. Death from inanition, pneumonia, heart failure. OPHTHALMOPLEGIA. This is a rare disease due to an atrophy of the nuclei of the nerves moving the eyeball. The muscular apparatus of the eye consists of external mus- cles moving the eyeball : Recti and obliqui and levator palpe- brae. Internal muscles moving the iris : Dilators and constrict- ors. Each of these may be affected alone or together. ( externa. Ophthalmoplegia j interna Ophthalmoplegia Externa. Symptoms. Gradually increasing loss of power in all the muscles of eyeball. One or more muscles at first, then others, till all are affected. Result, ptosis. Various forms of strabismus, nystagmus, and finally immobility of eyeball. Double vision. Ophthalmoplegia Interna. Symptoms. Loss of reflex to light. Occurs as a symptom in locomotor ataxia and general paresis. Diagnosis. From paralysis of single nerves, III. nerve or VI. nerve, by the fact that such disease is unilateral and all the l6 DISEASES OF THE NERVOUS SYSTEM. muscles supplied by the single nerve are involved, others remain- ing unaffected, and by the fact that the pupil is always affected. PROGRESSIVE MUSCULAR DYSTROPHY. This is a primary muscular disease which results in atrophy and paralysis. It is commonly mistaken for chronic anterior poliomyelitis or progressive muscular atrophy, but differs from this in causation, symptoms, and pathology. Causation. It is an hereditary affection, or a disease of devel- opment or of nutrition. It develops in several children in same family with same or various types. Pathology. The lesion is an essential and primary change in the muscle fibres. 1. Individual fibres become hypertrophied. The nuclei of the muscle fibres are increased in number. Then vacuoles appear as evidence of degeneration and fibres split up. At the same time there is an increase in connective tissue about the muscle fibres. Sometimes there is a development of fat between the muscle fibres. 2. Subsequently to the hypertrophy and sometimes without it atrophy of the muscle fibres occurs with same development of fat and connective tissue or without it. Appearance during hypertrophy is a very fat limb in which muscles are really weak ; during atrophy is a very thin limb in which muscles are very weak or even totally paralyzed. Symptoms. In all forms there develops a progressive simulta- neous weakness and atrophy of the muscles affected going on slowly to complete paralysis. The consequences of such paraly- sis are evident in size, posture, and deformities, use, motion, and gait. No fibrillary twitching vs. progressive muscular atrophy. No R. D. vs. chronic anterior poliomyelitis. No sensory disturbance, bladder, or rectal, or trophic skin changes. Various types of the disease classified by Erb : I. Infantile muscular dystrophy. i. Hypertrophic in type. Pseudo-hypertrophy fat only. True hypertrophy, muscle also. DISEASES OF THE NERVOUS SYSTEM. 17 2, Atrophic type. In limbs only. In limbs and face also. II. Adult muscular dystrophy, with similar classes. 1. INFANTILE MUSCULAR DYSTROPHY. HYPERTROPHIC FORM. i. Pseudo-hypertrophic Paralysis. Children aged from two to eight affected, males more than females. Only twenty-five per cent, occur after twenty years. Several in one family. Begins with difficulty in gait. Cannot walk, go up-stairs, or get up. Muscles of back atrophied, and calves of legs hypertrophied. Also infraspinatus and deltoid hypertrophied. Other muscles atrophy, pectorales, latissimus dorsi, triceps, and muscles of thighs. Posture, shoulders far back. Gait is waddling and mode of rising by climbing up the legs due to paralysis of extensors of hip is characteristic. Finally inability to sit up from paralysis of trunk. After paralysis has occurred shortening of muscles follows and deformities, talipes equinus and curvature of spine. No R. D. Knee-jerk normal, then weak. Sensation and sphincters not involved. Death is due to some intercurrent malady, occurs between twelve and twenty years of age. Only treatment is exercise. 2. True Hypertrophic Paralysis (juvenile muscular atrophy). Develops in children six to ten. Several in a family. Begins with progressive weakness of muscles. Muscles affected with hypertrophy are, deltoid, infraspinatus, muscles of forearm, sartorius, gastrocnemii. Muscles which atrophy are, pectorales, latissimus dorsi, ser- ratus magnus, biceps, coracobrachialis, supinator longus, adduc- tors of thighs, glutei and back muscles ; finally calf and peronei. Gait, posture and deformities are characteristic. No fib- rillary contraction. No R. D. Knee-jerk slowly diminished. No disturbance of sensation or of sphincters. 3. Atrophic Type in Body and Limbs (hereditary muscular atrophy). Same features, except entire absence of hypertrophy. Develops from eight to ten years. 18 DISEASES OF THE NERVOUS SYSTEM. 4. Atrophic Type in Limbs and Face (infantile muscular atro- phy ; Landouzy Dejerine type). Face is often first affected. When face is involved the zygomatic muscles are affected first ; loss of naso-labial fold ; flat mask-like face ; lower lip pro- jects ; orbicularis is affected ; lips open ; labials can't be spoken. Sometimes orbic. palpebrae weak. Facial muscles atrophy slowly. The other muscles of the body are affected in succession much later, pectorals, latissimus dorsi, biceps and triceps. Del- toids may be hypertrophied. Back muscles and extensors of thighs are invaded. Gait, posture, same as in other types. II. ADULT MUSCULAR DYSTROPHY. Any of these forms may occur in adults. Usually a family history can be obtained. Usually develops about age of eigh- teen, sometimes not till thirty. Some muscles are hypertrophied others atrophied as in infantile types. THE CENTRAL GRAY MATTER OF THE SPINAL CORD AND ITS DISEASES. The portion of gray matter lying behind the anterior horn, and adjacent to the central canal of the spinal cord and extend- ing backward to the posterior horn, is made up of gelatinous gray substance and of scattered nerve-cells with a plexus of fibres. It contains one long column of flask-shaped cells the column of Clarke in its posterior median part ; and an irregular column of small cells in its lateral part the intermedio-lateral column. The majority of these cells differ from the cells of the anterior horn, in not having a long axis cylinder process which enters a nerve. They have numerous branching processes, some send- ing a long branch to the other side through the anterior com- missure, others sending a branch out into the antero-lateral column where it bifurcates, turning up and down, and in its course gives off collaterals, which enter the gray matter at vari- ous levels. These cells thus form an associated system within the cord. The function of the central gray matter is to preside over, i, vasomotor tone ; 2, nutrition of all parts ; 3, visceral activity, in- cluding digestion and excretion, and the activities regulated by the sympathetic system. DISEASES OF THE NERVOUS SYSTEM. 1 9 i i. Vaso-motor innervation is a reflex matter requiring centres with sensory and motor nerves. Gaskell has proven that these lie in the central gray matter and are joined by fine nerve-fibres which pass in the nerve-roots through the two horns of the cord. The regulation of the flow of blood in accordance with the need of an organ is governed here. 2. The proper degree of metabolism necessary for nutrition in the skin, bones, and joints and muscles, or for repair of tissue, is under the control of nerves whose centres are in the central gray matter. 3. The sympathetic system of nerves presides directly over di- gestion, circulation, secretion, and excretion, but is in turn con- trolled by spinal centres which lie in the entire length of the spinal cord in the central gray matter. See Gowers, I., pp. 205 to 209. The central gray matter receives sensory impulses of pain and temperature sense and transmits these for some distance on their way upward after they reach it through the posterior nerve- roots ; each segment of the cord being related to its own part of the surface as shown in the table. All these functions are disturbed in diseases of the central gray matter. SYRINGO-MYELITIS. Pathology. This is a rare disease, of congenital origin, charac- terized by a development of gliomatous tissue in the gray matter around the central canal, which subsequently extends outward involving the entire central gray matter, and then degenerates and liquefies, leaving a cavity in the spinal cord. Such a cavity may extend through a part of the cord, or through its entire length ; varying in size at different segments and thus destroy- ing more or less of the gray matter. Its usual situation is in the lower cervical and upper dorsal regions. The disease may invade the anterior horns of the cord, causing the symptoms of chronic anterior poliomyelitis. It may invade the posterior horns and columns, causing symptoms of posterior sclerosis. Symptoms. i. Loss of the sensations of temperature and pain while the sensations of touch and location are retained. The dis- tribution of this sensory disturbance depends on the location of the disease, e.g., if the left hand and forearm only are thus affected the disease must be limited to the left side of the cervi- 20 DISEASES OF THE NERVOUS SYSTEM. cal region of the cord in its lower third, which receives sensations from these parts. Such disturbance of sensation may be exten- sive, involving irregular areas of the body. It is never symmet-^ rical on both sides. 2. Vasomotor and trophic symptoms. Cyanosis, oedema, blueness of extremities, with lowering of temperature, ulcers, bul- lous eruptions, sweating, thickened or glossy skin, defective growth of the nails, great brittleness of the bones leading to re- peated fractures, and joint affections, also progressive atrophy of the muscles. These occur usually in one limb only. 3. Disturbance in and loss of control over the action of bladder and rectum, and loss of sexual power are present when the lumbar region of the spinal cord is invaded. 4. Paralysis of the spinal muscles with curvatures of the spine. Course of the disease is chronic, with slow progress till the symptoms are developed, often including the symptoms of chronic anterior poliomyelitis. It then remains stationary, but if it ad- vances upward and invades the medulla, death may occur at any time from paralysis of the heart and respiration. The prognosis is bad and no treatment can stop the course. When tumors destroy the central gray matter or hemorrhages occur in it, the same terminal symptoms may be expected as in syringo-myelitis. THE POSTERIOR HORNS OF THE CORD. This portion of the cord is made up partly of gelatinous mat- ter which occupies its extremity, and partly of a fine plexus of nerve-fibres, in which small cells are irregularly scattered. The function of the posterior horn is to receive the impulses coming in through the posterior nerve-roots, and to transmit such im- pulses in various directions. These are the sensations of touch, temperature, pain, pressure, and location, and of the muscular sense. Each nerve of sensation gives off numerous branches on en- tering the cord, and finally terminates in a brush-like expansion of nerve fibrils which surrounds some nerve-cell, or in the plexus of nerve-fibrils which make up a fine felt-like tissue in the pos- terior horn. Any fibre after entering the posterior nerve-root may pass directly into the posterior horn, or may turn up or down in the white matter near the horn and enter the posterior DISEASES OF THE NERVOUS SYSTEM. 21 horn at some level other than that of its entrance. The posterior horns are continuous upward (through the medulla and pons) with the ascending root of the fifth nerve. The diseases of the posterior horn will be considered with diseases of the posterior roots and columns, as they uniformly coincide. THE WHITE COLUMNS OF THE SPINAL CORD AND THEIR DIS- EASES. The gray matter of the spinal cord is surrounded by white tissue made up of anterior and posterior nerve-roots and of nerve- fibres passing up or down the cord for longer or shorter dis- tances. The white columns contain therefore : 1. Fibres joining the skin, joints, muscles, and viscera to the gray matter of the spinal cord and entering the various segments through the anterior and posterior nerve-roots. 2. Fibres connecting the various segments with one another. 3. Fibres joining the various segments with the brain. The white matter can be divided into different columns by observing the process of development different columns develop at different periods of foetal life ; or by studying the process of disease different diseases select different columns. These columns and their diseases are as follows : THE MOTOR COLUMNS. 1. Anterior median column. 2. Lateral pyramidal column. At the lower limit of the medulla each anterior pyramid di- vides into two parts; one part passes directly on into the an- terior median column of the cord ; the other part crosses over to the opposite lateral column of the cord, lying near to the gray matter in the angle between the anterior and posterior horn. As the fibres making up these columns pass down the cord they turn into the anterior gray horns of the different segments each column becoming smaller the lower it goes. The anterior median column is exhausted at the lower dorsal cord and, there- fore, does not exist in the lumbar region. The lateral pyramidal column extends to the lowest segment of the cord. These col- umns transmit motor impulses from the motor cortex of the brain and from the motor ganglia of the brain to the spinal motor centres. These columns also contain fibres whose origin is in 22 DISEASES OF THE NERVOUS SYSTEM. the pons and cerebellum, which pass with the motor fibres from the brain and terminate in the anterior horns of the cord. They also contain fibres of association passing between vari- ous segments of the cord. All these sets of fibres degenerate downward. The area of degeneration is less in extent when the lesion is in the brain than when it is in the cord itself. LATERAL SCLEROSIS. Lateral sclerosis is a chronic sclerotic process affecting the lateral pyramidal columns of the spinal cord. It may be primary and is then bilateral. It may be secondary to other diseases in the brain or cord which separate the fibres of the motor tract from their centres of origin and nutrition in the brain cortex. Such diseases are : 1. Tumors, softening or hemorrhage in the brain, destroying the motor tract in one hemisphere, in which case the secondary sclerosis is found in the anterior median column and the oppos- ite lateral pyramidal tract. 2. Congenital maldevelopment of the brain and hydroceph- alus, affecting both motor tracts, in which case both anterior me- dian and both lateral columns are sclerotic. 3. Any lesion in the spinal cord, either unilateral or bilateral, or compression of the cord by disease of the vertebrae, in which case the sclerosis only appears below the level of the lesion, and its extent is greater in area than in i or 2. Pathology of Sclerosis. i. An increase in the thickness of the connective-tissue framework which supports the nerve-fibres. 2. A primary degeneration or a secondary destruction of the axis cylinder in each nerve-fibre, resulting in its swelling, seg- mentation, fatty degeneration, and final absorption. The result is to reduce the number of fibres in any column of the cord, or even to destroy them entirely, the place of the fibres being filled by connective tissue. Symptoms of Primary Lateral Sclerosis, or Spastic Paraplegia. A weakness and stiffness in motion, beginning in the legs and ascending, finally involving the arms. The muscles affected do not atrophy rapidly, as their spinal centres are not diseased. Their reflex and mechanical excitability is increased, as the spinal centres are no longer inhibited by brain impulses. Hence increased knee-jerk and ankle clonus are present. They be- come rigid from the increased spinal activity. Hence the gait DISEASES OF THE NERVOUS SYSTEM. is at first "spastic" (toes drag, knees overlap, motion stiff), finally, when paralysis is complete, the legs are drawn up, knees overlapping and so rigid as to be incapable of passive motion. There are no electric changes in the muscles. The action of the bladder is imperfectly controlled, and finally involuntary emptying of the bladder at intervals or retention of urine occurs. Constipation is obstinate. In some cases of pri- mary lateral sclerosis the bladder and rectum are not affected. The vascular tone is decreased toward the close of the disease and nutrition is impaired. There are no sensory symptoms. Course of the Disease. The symptoms develop slowly and in- crease until, after many years, permanent paralysis has de- veloped. Secondary Lateral Sclerosis presents the same symptoms on one or both sides, but the symptoms develop more rapidly according to the nature of the primary disease. Diagnosis between lateral sclerosis and anterior poliomyelitis : Lesion in pyramidal tracts. Paralysis usually on both sides equally, in legs, or in legs and arms, never in arms alone. All muscles are about equally affected. No muscles are entirely normal. Muscular tone is heightened. Tendency to rigidity appears. Reflex excitability is increased. A trofliy is absent, or is slight ; and merely due to disuse, hence is gradual in prog- ress. It affects the entire limb. Electric contractility is unchanged. Vascular tone is diminished ; cyanosis and oedema may occur. Paralyzed limb is cold, and sweat may be increased. Trophic disturbances in the skin are not infrequent. The control over the bladder and rectum may be diminished or lost. Lesion in anterior gray horns. Paralysis may be limited to any single limb, and rarely affects both limbs equally. Certain groups of muscles only are af- fected. Others escape wholly. Muscular tone is diminished. Muscles are relaxed. Reflex excitability is lost. Atrophy is always present in the paral- yzed muscles. It advances rapidly, and may become extreme. Electric contractility is changed. Reac- tion of degeneration is present within two weeks of the onset. Vascular tone is diminished, but cedema does not occur. Paralyzed limb is cool, but sweat is not increased. Trophic disturbances in the skin do not occur. The control over the bladder and rectum is not impaired. Treatment. None. [Read Strumpell on spastic spinal paral- ysis and on compression myelitis.] 24 DISEASES OF THE NERVOUS SYSTEM. AMYOTROPHIC LATERAL SCLEROSIS. This is a chronic disease affecting the entire motor system of the spinal cord and cerebral axis, both the groups of cells in the anterior horns and medulla and pons, and also the lateral pyra- midal columns in the cord and in the medulla and pons being affected together. The extent of the sclerosis is greater in the cord than in primary lateral sclerosis, as the white column which lies between the pyramidal tract and the gray matter (the lateral limiting column) is also sclerotic in this disease. The changes in the anterior horns are the same as in chronic anterior polio- myelitis. Symptoms. The symptoms present features similar to those of chronic anterior poliomyelitis and of extensive secondary lateral sclerosis. Weakness, paresis, and atrophy begin in one or both arms and hands and increase slowly. The muscles of the hands and the extensors of the wrist, the deltoid and triceps, are the muscles chiefly affected. The electric contractility is di- minished, and finally reaction of degeneration appears. The muscular irritability and reflexes are much increased. Finally contractures result. Gradual onset of spastic paraplegia in the legs occurs a few months after the arms are affected. Spastic gait develops with increased reflexes. In the final stage the legs are totally para- lyzed. There are no sensory disturbances, and bladder and rectum are usually under good control. After several years symptoms of bulbar paralysis gradually develop, with paresis and atrophy of face, tongue, and throat, and death occurs from respiratory paralysis. Occasionally the bulbar symptoms appear early. The course is a slow one. The disease may be arrested, but recovery is impossible. Diagnosis from myelitis of the cervical region and from syrin- go-myelitis by the absence of sensory symptoms ; from anterior poliomyelitis chronica by increased mechanical and reflex excit- ability in muscles atrophied, and by development of spastic gait. Treatment. N one. DISEASES OF THE NERVOUS SYSTEM. 25 THE SENSORY COLUMNS. 3. Posterior Lateral Column, or Column of Burdach. 4. Posterior Median Column, or Column of Goll. 5. Marginal Column, or Column of Lissauer. These columns are made up chiefly of sensory fibres which enter the cord in the posterior nerve-roots. They also contain fibres of association between different segments of the cord. Their subdivisions will be better understood by a study of the course of the posterior nerve-roots. The posterior nerve-roots contain two sets of fibres. The ma- jority arise from the cells of the posterior spinal ganglia. The minority arise from the so-called tactile corpuscles of the ex- tremities. Each spinal ganglion cell has two branches, or two divisions of one branch ; one going out to the surface, the sen- sory nerve ; the other going in to the cord, the posterior nerve- root. The cell in the ganglion nourishes both branches, and if either branch is separated from its cell it degenerates in its entire length. The sensory cranial nerves (X., IX., V.) arise from similar ganglia (jugtilare Gasserian). The posterior nerve-root enters the cord opposite to the apex of the posterior horn and then divides into two bundles, a me- dian bundle and a lateral bundle. (i) The median bundle containing large fibres enters the col- umn of Burdach, forming its root zone or lateral zone. Here a few fibres turn downward into the segment next below, and end in the posterior horn ; but the large majority of fibres turn up- ward to go to higher segments. Some of these soon enter the inner side of the posterior horn (short fibres). These lie near the horn in the lateral zone. Others pass up through several segments (medium fibres). These lie nearer to the median line and in the upper cord are adjacent to the column of Goll, form- ing the middle zone of the column of Burdach. The remainder pass all the way up to the medulla (long fibres), lying at first in the hinder zone of the column of Burdach and later forming the column of Goll. For as each root, from below upward, enters the cord it displaces inward and backward the fibres already as- cending ; so that the higher the level the larger the number of ascending fibres. In a cross section of the cord in the upper cervical region the long fibres which have come from the lumbo- 26 DISEASES OF THE NERVOUS SYSTEM. sacral region occupy the column of Goll, the sacral fibres lying behind the lumbar ; the long fibres from the dorsal region oc- cupy the hinder zone of the column of Burdach ; the long fibres from the cervical region occupy the middle zone of the column of Burdach. It is evident that there is no physiological distinc- tion between the columns of Goll and Burdach. In the anterior part of both columns near the gray commissure lie association fibres and commissural fibres. It is thus evident that the median bundle of posterior nerve-root fibres constitutes the columns of Burdach and of Goll. The final termination of these fibres is as follows : Each fibre on entering the cord bifurcates, a short branch turns down, a long branch turns up. The long branch in its course upward gives off collateral branches which pass into the gray matter of the posterior horn, and finally the branch itself ends there. In all cases the termination is by means of a brush-like expansion of nerve-fibrils. The short fibres end in the fine net-work mak- ing up the substantia gelatinosa of Rolando in the posterior horn, and about the cells of the posterior and central gray mat- ter. The medium fibres end in a net-work which surrounds the cells of the column of Clarke in the central gray matter. A few fibres pass forward to the anterior horn and to the opposite side through the posterior gray commissure. The long fibres pass up to the nuclei gracilis and cuneatus in the medulla. (2) The lateral bundle of the posterior nerve-root consists of both large and small nerve-fibres. Many of these pass directly into the gray matter of the posterior horn, where some end in a net-work of fibres about the cells of the gelatinous substance, or deeper in the horn ; and others pass forward and cross over in the gray commissure to the opposite side, where they turn out- ward into the antero-lateral column or backward into the col- umn of Goll. The smaller fibres bifurcate on entering the cord and turn down and up, forming the column of Lissauer, in which they pass but a short distance and then turn into the horn. This column is of uniform size through the cord and hence can- not contain any long fibres. 6. Antero-lateral Ascending Tract or Column of Gowers. In the antero-lateral column of the cord lying on the periphery just in front of the direct cerebellar column is a small tract which as- cends through the cord and enters the formatio reticularis of the medulla, where it appears to end in the gray cells of this DISEASES OF THE NERVOUS SYSTEM. 27 formation. It begins in the lumbar region, and increases in size as it ascends, receiving fibres from the cells of the central gray matter. It degenerates upward. It has been supposed to con- vey sensations of temperature and pain upward after they have passed through the central gray matter. 7. Direct Cerebellar Column. This column lies on the lateral periphery of the cord just outside of the pyramidal tract and be- hind the antero-lateral ascending tract. It is very small in the upper lumbar region, becomes larger in the dorsal region, and is of considerable size in the cervical region. Its fibres come from the cells of the column of Clarke in the central gray matter. It passes into the restiform body in the medulla and through this into the cerebellum, where it ends in the vermiform or middle lobe. It is supposed to convey sensations of equilibrium in the act of walking. It is evident that the sensory fibres from the posterior nerve- roots are distributed to many different columns of the spinal cord, and even in the medulla have numerous different connec- tions. This anatomical fact may be associated with the physio- logical fact that one sensation is capable of producing several different effects, e.g., a burn causes a reflex withdrawal of the part burned, vascular changes, and a process of repair, sensa- tions of heat, touch, and pain, accurately localized, followed by conscious effort to protect the part : e.g., stumbling in the act of walking causes reflex balancing movements involving motions of the entire trunk and arms to reestablish the centre of gravity or protect against fall, also conscious sensation of unstable position, possibly vertigo, quickened respiration, action of ocular muscles and head to observe danger, sensation of contact, possibly pain, in the toes, and corresponding vascular changes locally, and finally voluntary effort to correct position after an appreciation of all the various sensations received. We distinguish conscious sensations of contact, temperature, pain, muscular sense, including pressure and position, and un- conscious sensations, which set up reflex and automatic acts, vascular changes, variation in thermic and nutritive processes, and changes in muscular tone. These all enter by the posterior nerve- roots, and set up activities in the central nervous system. 28 DISEASES OF THE NERVOUS SYSTEM. LOCOMOTOR ATAXIA. This is a chronic disease of the sensory part of the nervous system, the posterior nerve-roots and the posterior columns of the cord being diseased. It is also called tabes dorsalis, or posterior spinal sclerosis. Pathology. There is a degenerative neuritis of the posterior nerve-roots, and sometimes of the sensory part of the peripheral nerves. There is a sclerosis of the posterior columns of the spinal cord, beginning in the lateral or root zone of the column of Burdach and in the column of Lissauer, extending thence to the middle zone of the column of Burdach, then to the column of Goll, and finally to the hinder zone of the column of Burdach. Thus both posterior columns are eventually diseased in their entire extent. The disease usually begins in the lumbo-sacral region and extends upward through the cord. It is many years before it invades the cervical region or destroys the entire area of the posterior columns. The terminal net-work of nerve-fibres in the posterior gray matter, and especially about the column of Clarke, is destroyed by the disease. Theories of the disease: (i) It is a primary sclerosis of the posterior columns of the cord. (2) It is a sclerosis of the root- zone, due to disease of the vessels entering this zone. (3) It is a primary disease of the cells of the posterior spinal ganglia, with secondary degeneration of the sensory fibres entering the cord from the ganglia, and compensatory sclerosis in their course. Etiology. It is a disease of adult life, persons under twenty- five rarely being affected, and it is rare among women. The chief predisposing cause is syphilis, which precedes it in seventy per cent, of the cases. The exciting causes are great physical exer- tion, exposure to cold and wet, and alcoholic and sexual excesses. Symptoms. The symptoms of the disease are very numerous, but appear in succession. They may be classified according to the time of their appearance. There is a stage of pain, a stage of ataxia, and a stage of paralysis. Symptoms in Stage of Pain. Paraesthesiae. Numbness, formication, sensation of dead ex- tremities, cotton or pins in soles of feet and fingers, coldness, itch- ing of anus and scrotum or of other parts. Pain. Short, sharp, cutting, boring. Deep pain ; comes in DISEASES OF THE NERVOUS SYSTEM. 29 attacks, one second to one-half minute repeated, or in severe attacks for several hours or days with intermissions, rarely con- tinuous attacks. Begins in thighs and legs. Pain is a prominent symptom early, but may continue through all stages. It may be mistaken for rheumatism or sciatica, but its character is different. It is the same as in alcoholic multiple neuritis, but there tender- ness exists. There is no relation between intensity of pain and degree of ataxia. As disease advances upward the pains extend. Pain may be absent or insignificant in some cases, especially in cases beginning with optic-nerve atrophy. Pain in the small of the back and loins of an aching character may occur. Girdle sensation or sensation of tightness and pressure in- tense and severe, about the legs and body. This ascends gradu- ally as the disease advances. Loss of knee-jerk, called Westphal's symptom. Imperfect control of bladder. Slow urination. Slight drib- bling, and hasty urination. Finally control is very imperfect and may be painful. This may be a dangerous complication, since death from cystitis occurs. Impotence ; occasionally priapism and sexual excitement pre- cedes this. Constipation ; usually obstinate throughout. Loss of pupil reflex to light, the reaction in accommodation being preserved Argyle-Robertson pupil. Contracted pupil, " myosis spinalis," is frequent but not constant. Symptoms in Stage of Ataxia. In addition to those of first stage there develop : Anaesthesia and analgesia. Sense of pain impaired and de- layed. This may be tested with faradic brush. It prevents in- juries from being perceived ; hence ulcer of foot and Charcot joints occur as complications. Hence, guard against accidents in giving hot baths, blisters, etc. Hyperalgesia. Sensation of pain may be produced by any touch, and pain is felt severely. This occurs in a few cases early in the disease. Change in temperature sensation. Cold felt keenly and heat less than normal. Complete anaesthesia develops late in the disease in the ex- tremities. 30 DISEASES OF THE NERVOUS SYSTEM. Impairment of muscular sense. Muscular sense is the sense by which the situation and movements of the limbs are appreci- ated, and pressure and weight are felt. Not same as effort sense. Imperfect perception of weight and pressure is a symptom ob- served late. Situation of limbs is imperfectly perceived. Hence, one means of perfect guidance of limbs is removed. Hence, patient walks badly in the dark, and cannot touch objects accu- rately with eyes closed ; hence, he watches his own motions aid- ing his muscular sense by sight. Therefore a blind ataxia is the most helpless of all. Ataxia is imperfect co-ordination of muscular action. For every compound act a regular succession and proper degree of motions are needed, e.g., closure of fist, walking. This regula- tion is largely automatic and is carried on in subcortical cen- tres, which receive unconscious sensations through the pos- terior nerve-roots. It may be voluntary, by an effort of attention, and is so at first, for all motion, and always for highly complex motion, e.g., writing. Hence ataxia of movement may occur in many diseases. It is a prominent symptom in locomotor ataxia. Romberg's symptom swaying when standing with eyes closed. Ataxic gait legs wide apart, feet lifted too high, and planted too forcibly, steps being of irregular length and body imperfectly balanced. Imperfect use of hands in dressing, writing, etc. Irregular contraction of muscles on effort. Imperfect muscular tone. Tests of ataxia. Stand with eyes closed, walk, turn suddenly or walk backward ; touch heel to toe, or heel to knee ; touch finger to nose or both fingers with eyes closed ; pick up pin ; button clothes. Symptoms occasionally present, due to complication of neuritis in various nerves. Optic nerve atrophy, with progressive blindness develops in twenty per cent, of the cases. Optic disc looks white, then gray. Arteries appear small and walls thin. Visual field is contracted for colors and for light. Finally total blindness oc- curs. Paralysis of the ocular muscles. VI. n. paralysis : convergent strabismus, with contracted pupil. III. n. paralysis ; divergent strabismus, with dilated pupil and ptosis. Nystagmus rarely occurs. DISEASES OF THE NERVOUS SYSTEM. 31 Deafness develops in a few cases from atrophy of auditory nerve. Crises (i) gastric ; sudden vomiting with pain, for several hours, even for days. Great prostration follows. Rectal feeding necessary. Intestinal and rectal crises with diarrhoea and tenes- mus have been observed. (2) Laryngeal ; sudden severe cough, with spasm of larynx and suffocation. (3) Cardiac ; attacks of angina pectoris. All due to a complicating peripheral neuritis in pneumogastric nerve. These symptoms are quite exceptional. Trophic disturbances are more common in stage of ataxia. Charcot joints. Knee, elbow, ankle, wrist. Enormous swell- ing with effusion without pain. Erosion of ends of bones and destruction of articulation. Due to injury. Perforating ulcer of foot, caused by a corn, or a subcutane- ous haemorrhage, or a caries of bone neglected. Rarefication of the bones with production of fractures. Irregular muscular atrophies develop late in the disease. Herpetic eruptions and pemphigus. These are due to a combination of causes, chiefly to a loss of pain sense which prevents injuries from being perceived, or to a complicating peripheral neuritis. Symptoms in Stage of Paralysis. General nutrition remains good, but ataxia becomes so ex- treme as to render patient helpless and confine him to bed. Control of bladder completely lost, and urine dribbles con- stantly. Accidents produce injuries, and trophic disturbances follow. Hence patients die of bedsores, cystitis, exhaustion, or of complicating pneumonia. Course of the disease is chronic through the three stages, last- ing twenty to forty years. Usual mode of onset is with pain, loss of knee-jerk, bladder trouble, impotence, and ataxia. Occasional modes of onset : (i) blindness, loss of knee-jerk, imperfect gait, numbness, but no pain. (2) Gastric crises at intervals, loss of knee-jerk, then pain and ataxia. (3) Various forms of strabismus, myosis, then ataxia of arms. There are remissions in the symptoms and complications may subside, but no true arrest occurs or recovery, after the stage of ataxia has begun. 32 DISEASES OF THE NERVOUS SYSTEM. Diagnosis. Early, by means of pains, fatigue, loss of knee- jerk, and Argyle-Robertson pupil. Late, by ataxia and bladder disturbance. Diagnosis from multiple neuritis. See page 8. Treatment. Moderate exercise, avoiding all fatigue. Good general diet without special restrictions, which weaken patient. Spinal douches, tepid or cool, never extreme. Massage. Prac- tise in fine movements to overcome ataxia. Medicines arsenic, nitrate of silver, ergot. Treatment of pain by antipyrine, etc., gelsemium, opium, fara- dization, hot applications. Of crises by counter-irritation and morphine. Of optic atrophy by strychnine. Of trophic disturb- ances by rest and apparatus. COMBINED SCLEROSIS. This is a Sclerosis of the Lateral and Posterior Columns {rare). (1) Congenital cases. FriedreicJis Hereditary Ataxia is due to defective development of the lateral and posterior columns. It occurs in several members of a family, and is hereditary. Symptoms. As the children grow up they are found to be awkward. They walk badly, and do not use arms well. Re- flexes are lost, exceptionally exaggerated. Dull pains in legs, not lightning in character. No bladder symptoms, and no trophic changes, and no crises. Ataxia is marked and goes on to actual paralysis. Speech may be thick and nystagmus present. The condition is a chronic one lasting during life. (2) Acquired cases. Ataxic Paraplegia of Gowers. Etiology. Occurs in males chiefly, between thirty and forty years of life. Not after syphilis, but after exposure to cold or sexual excess. Possibly after concussion of spine. Symptoms. Slow onset of weakness and ataxia together. Un- due fatigue, unsteady gait. Romberg symptom. Dull pain in back and legs, no lightning pains. Reflexes increased. Knee- jerk high, ankle clonus present. Sexual power lost. Sphincters less impaired than in tabes. Eye symptoms very rare. Tremor of face and speech sometimes develops. Differs from tabes in fact that the nerve-roots are not in- volved. Course. Weakness increases slowly to paralysis. Rigidity DISEASES OF THE NERVOUS SYSTEM. 33 soon develops, and contractures. Death occurs from complica- tions. THE ASSOCIATION COLUMNS. 8. Antero- Lateral Column. There is a large collection of nerve- fibres forming a white column lying adjacent to the. gray matter of the cord, in front and inside of the pyramidal tract, and inside of the direct cerebellar and antero-lateral ascending tracts, ex- tending as far forward as the anterior nerve-roots. A portion lying next to the gray matter has been named the lateral limiting layer. This column contains a few fibres which degenerate all the way upward to the medulla, and it is possible that some sensory impulses are transmitted through it. The major part of the fibres are, however, short, and serve to connect the various segments of the cord with one another. In it pass the majority of the " association fibres " of the cord which harmonize the ac- tion of different parts. 9. Anterior Column. This lies between the exit of the anterior nerve roots and the anterior median column. It has the same function as the antero-lateral column, and like it ends in the formatio reticularis of the medulla. There are very many polygonal cells scattered through the gray matter in both horns and in the central gray which send out to these columns an axis cylinder process which, on entering the column bifurcates, sending one branch down and the other upward. These branches give off collaterals in their course which pass into the gray matter at various levels and terminate in brush-like expansions. The original branches terminate in the same way after having a longer or shorter course. Thus the majority of the fibres in these columns are true association fibres. There are a few such fibres also in the portion of the posterior columns ad- jacent to the gray commissure. SECONDARY DEGENERATIONS. When the cord is divided by an injury or by transverse my- elitis there results a degeneration in the various columns. The anterior median and lateral pyramidal columns degenerate downward for their entire length. There is also a short tract of degeneration downward in the lateral zone of the column of Bur- 34 DISEASES OF THE NERVOUS SYSTEM. dach. The anterior and antero-lateral columns degenerate down- ward for a short distance. The columns of Burdach and Goll and Cowers and the direct cerebellar column degenerate upward through their entire length. The columns of Lissauer and the anterior and antero- D lateral columns degenerate upward for a short distance. Such degenerations are due to the fact that the transverse lesion cuts off the individual fibres from their nutrient cells, and hence the distal end degenerates, the fibres nourished by cells above the lesion degenerating downward and those by cells be- low the lesion degenerating upward. MYELITIS. This is an inflammation of the spinal cord involving an entire segment, both gray and white matter. Pathology. Cord looks normal, but feels soft at points ; or may break in two and be soft enough to be fluid. On cutting it the cut surface swells out as if semi-fluid ; the gray matter looks red and capillary hemorrhages are seen ; the limit of white and gray is indistinct. Microscopically. Large numbers of inflammatory corpuscles everywhere. Nerve-cells and fibres swollen and degenerated, granular and disappearing or atrophied. Neuroglia cells in- creased. Deiter's spider cells present. Fatty and granular cells everywhere as evidence of degeneration. Vessels are distended with blood and ruptured; walls may be infiltrated and thickened- Secondary degeneration as already enumerated. Etiology. Males more than females. Soldiers, porters. Age ten to forty. Exposure to cold. Over - exertion. Falls and blows. Concussion of cord. Sexual excesses. Menstrual sup- pression. After confinement. Injuries of the cord. Compres- sion of the cord by disease of spinal bones or tumors. Secondary to acute infectious diseases. Syphilis and chronic alcoholism. Varieties, General. Entire cord affected ascending or de- scending. Disseminated. Various segments at different levels affected. Transverse. One or two segments at one level affected. Symptoms. (i) Direct, due to destruction of cord tissue. i. Motor. Paralysis, atrophy. R. D. Loss of tone in mus- cles. DISEASES OF THE NERVOUS SYSTEM. 35 2. Reflex. Loss of spinal reflexes. Paralysis of the bladder and rectum, impotence. 3. Sensory. Numbness. Pain. Paraesthesia, anaesthesia. Hyperaesthesia at upper level of lesion. Pain and tenderness of back to heat. 4. Vaso-motor and trophic. Imperfect circulation. Skin cold. Sweat profuse. Bed-sores on buttocks, sacrum, and heels. The distribution of the direct symptoms depends on the ex- tent of the lesion. If general they are universal. If dissemi- nated they are scattered. If transverse they are limited to one level. Diagnosis of level from situation of symptoms, motor or 'sen- sory, see table, page 10. Symptoms. (2) Indirect, due to cutting off of impulses to other parts. The cord transmits impulses to and from the brain. In disseminated and transverse myelitis tracts are broken, (i) Mo- tor tracts to parts below, hence secondary lateral sclerosis with its symptoms. (2) Sensory tracts from parts below, hence sec- ondary degenerations upward with their symptoms. Secondary symptoms are : 1. Rigidity and increased reflexes, contractures, spasms of legs, paralyzed muscles not atrophied and no R. D. 2. Loss of bladder control without bladder paralysis, priap- istn. 3. Imperfect sensation without incoordination. 4. Imperfect perception of pain, hence bed-sores from dirt, bed-sores over sacrum, glutei, heels, and ankles. Examples : In general myelitis, direct symptoms throughout body. In disseminated myelitis, direct symptoms in irregular areas, few indirect symptoms. In transverse myelitis, direct symptoms very limited, indirect symptoms below the lesion. (a) Cervical transverse myelitis, direct symptoms in arms, in- direct in legs. (b) Dorsal transverse myelitis, direct symptoms few, in trunk, indirect in legs, arms free. (c) Lumbar transverse myelitis, direct symptoms in legs, arms free, no indirect symptoms. Course of General Myelitis and Disseminated Myelitis. Acute or subacute, onset in two weeks after a cold or great strain or after 36 DISEASES OF THE NERVOUS SYSTEM. typhus, typhoid, small-pox, confinement, syphilis. Weakness in limbs. Pains in back and limbs. Prostration. Then paralysis. Pain and anaesthesia. Bladder and rectal symptoms. Then pa- tient is confined to bed and bed-sores develop. Slow course for a year to three years and occasionally gradual, imperfect recov- ery. Usually cystitis, bed-sores, or pneumonia and death. Course of Transverse Myelitis. Acute, onset after injury blow, fall, wound, dislocation of spine, or strain, causing hemorrhage in cord ; or from embolism of spinal arteries. Chronic, onset after spinal caries with deformity and press- ure, or tumor in spinal canal or cord. Course depends on pos- sibility of removing the cause. Diagnosis. Myelitis vs. multiple neuritis, see page 8. MYELITIS vs. MENINGITIS. Very rapid onset. Slower onset. Fever moderate. Fever high. Pain in back moderate, in limbs or body Pain in back and body and limbs very se- dull. vere, increased by motion. Hyperaesthesia slight in a band at upper Hypersesthesia of entire body and limbs level of lesion. very intense. Anaesthesia below lesion. No anaesthesia. No spasms or rigidity. Spasms of limbs and back with rigidity of back appear early. Paralysis total in some muscles with Paralysis only apparent ; due to fear of atrophy and R. D. pain on motion ; no atrophy. Sphincters paralyzed. Sphincters not affected. Bed-sores and cystitis. No bed-sores or cystitis. MYELITIS vs. HYSTERICAL PARAPLEGIA. Anaesthesia below lesion includes geni- Anaesthesia varies in level and genitals tals. never included. If thighs are paralyzed and atrophied re- When legs are paralyzed reflexes are ex- flexes are lost. aggerated. Usually some muscles atrophy and show Muscles rarely atrophy and R. D. never R- D. appears. Sphincters usually involved. Sphincters rarely involved. Diagnosis of level of lesion by distribution of anaesthesia, see table, page 10. Treatment of myelitis. When onset is acute remove cause, and use counter-irritation, ice-bag or warm douche. Keep at perfect rest in prone posi- DISEASES OF THE NERVOUS SYSTEM. 37 tion. Give sedatives and ergot, in early stage give purgatives, calomel, or salts. When case is chronic in onset or in course : Employ counter-irritation. Cups, blisters, cautery, ether spray ; but not in cases with tendency to bed-sores. Use baths, douches, tepid and cold, to spine. Keep up strength of patient by good diet, and regulate diges- tion. Use massage to the limbs hot baths for rigidity. Use interrupted galvanic current to atrophied and paralyzed muscles. Prevent cystitis by keeping catheters and parts clean and aseptic. Prevent bed-sores by careful padding or water-bed, by spong- ing with alcohol and alum-water. Treat cystitis by washing out the bladder as in surgery. Treat bed-sores by aseptic dressings, as in surgery. For pain apply heat or faradic brush to part. Give anti- pyrin, antifebrin, phenacetine, morphine, salicin, salicylic acid. For spasms apply heat to spine, or hot bath to legs, or cups. Give bromides. For rigidity, when beginning, pads and massage. For incontinence of urine pads of absorbent cotton, or wear urinal. Medicines in chronic myelitis : Iodide of potash, gr. x. to xx., t.i.d. Nitrate of silver in pill with kaolin, gr. % t.i.d. increased. Ergotin when congestion is suspected. Strychnine when an increase of reflex activity is not present. Phosphorus and arsenic as nerve-tonics. Use ung. hydrarg, and KI in large doses in syphilitic cases. HEMORRHAGE INTO THE SPINAL CORD. Hemorrhage into the spinal cord or into the membranes is a rare occurrence, and is almost always due to traumatism. The symptoms produced are those of sudden suspension of all spinal functions at and below the level of the hemorrhage. They are therefore identical with those of transverse myelitis, and the sud- den onset affords the only means of distinguishing the two dis- eases. 38 DISEASES OF THE NERVOUS SYSTEM. TUMORS OF THE SPINAL CORD. Tumors rarely grow in the spinal cord. They are usually secondary to tumors elsewhere. All varieties may occur. The symptoms produced are those of transverse myelitis of slow onset and characterized by extreme pain at the level of the tumor or in the sensory areas which correspond to the segment in which the tumor grows.. The only relief is. by operation. BROWN-SEQUARD'S PARALYSIS. Hemorrhages in the cord, tumors in or about the cord, and bony growths or callous, the result of injury, sometimes divide or compress one-half only of the cord. The symptoms resulting were first described by Brown-Se'quard, and hence the condition lias been named after him. This condition is as follows : (i) on the side of the lesion there is paralysis with increased reflexes, and sometimes a loss of muscular sense below the level affected, and a marked hyperaesthesia to touch and pain ; (2) on the side op- posite to the lesion there is no paralysis, but there is a loss of sensation of touch, temperature, and pain, and sometimes a de- velopment of bed-sores below the level of the lesion ; (3) at the level of the lesion there is a band about the body of anaesthesia, with another band of hyperaesthesia above it ; the band on the side of the lesion being a little higher than upon the opposite side. THE BRAIN AND ITS DISEASES. I. THE CORTEX OF THE CEREBRAL HEMISPHERES. THE cortex consists of gray matter spread out in a layer over the cerebral hemispheres, 3 mm. thick and about 200,000 sq. mm. in extent ; its amount varying greatly in different persons ; its development determining mental capacity. The development of fissures throwing the cortex into folds enables this large extent to be contained in the skull. The Microscopic Appearance of the Cortex. Cells arranged in layers. (1) Superficial or molecular layer ( T 1 7 ) small cells. Much neuroglia. (2) Layer of small pyramids (-j^) with many branches and short process. (3) Layer of large pyramids (^) with few branches and a long projection fibre process. (4) Layer of polymorphous cells (-fo) with many short branches and a short process. (5) Layer of fusiform cells ( T 2 ff ) with short branches and asso- ciation fibre process. Fibres traverse these layers giving off collaterals and form an intricate net-work throughout the gray matter. There are great variations in the structure of different regions. (See " Ouain's Anatomy," loth Ed., Vol. III.) The fibres arising from the cortex and constituting the white o o matter beneath it are (i) association fibres passing to some other part of the cortex ; (2) commissural fibres passing to the cortex of the opposite hemisphere ; (3) projection fibres passing to the basal ganglia, cerebral axis or spinal cord. Divisions of the Cortex into Lobes and Convolutions. Frontal lobe, 40 per cent. ; parietal lobe, 20 per cent. ; temporal lobe, 20 per cent.; occipital lobe, 17 per cent.; Island of Reil, 3 per cent, of extent of cortex. Landmarks on the Cortex. Fissure of Sylvius, fissure of Ro- 40 DISEASES OF THE NERVOUS SYSTEM. lando, iflterparietal fissure, parieto-occipital sulcus, calcarine fissure, eolloso-marginal fissure. CRANIOCEREBRAL TOPOGRAPHY. To find the fissure of Rolando, lay down a line from the root of the nose to the occipital protuberance over the top of the head and take a point 0.557 of the distance back upon tins line. This point will correspond to the upper end of the fissure. The fissure makes an angle of 67 with the median line just meas- ured. Hence if two strips of metal, fixed to one another at this angle be placed on the head with their junction upon the upper end of the fissure, when one strip is on the median line the other strip, pointing forward and downward, must lie over the fissure of Rolando. In its lower third the fissure becomes a little more vertical than the strip. The fissure is about three and a half inches long. To find the fissure of Sylvius, lay down a base line from the lower margin of the orbit to the auditory meatus. Lay down a second line parallel to the base line from the external angular process of the frontal bone backward one inch and a quarter and then measure upward one quarter of an inch ; this gives point one. Find the most prominent part of the parietal eminence and from it draw a line downward perpendicular to the base line, and on this take a point three-quarters of an incli below the eminence ; this gives point two. Join these two points and the line will lie over the fissure of Sylvius. The anterior limb of the fissure will be two inches behind the external angular proc- ess. The fissure of Sylvius is about four inches long. To find the parieto-occipital fissure, continue the line of the fissure of Sylvius to the median line. At their junction lies this fissure. Since all areas now open to surgical operation can be located with a definite relation to these three fissures, no further rules are necessary. Since in opening the skull it is customary to make a fenestra of at least an inch in diameter, and it is fre- quently necessary to enlarge the opening much more, a proced- ure in no way dangerous under aseptic conditions, there is no difficulty in recognizing the fissures and convolutions exposed if the rules are closely followed. Prior to the large incision of the scalp it is well to mark certain points upon the skull by the sharp point of a chisel, so that when the bone is laid bare sur- face landmarks may still be kept in view. DISEASES OF THE NERVOUS SYSTEM. 41 LOCALIZATION OF FUNCTIONS IN THE CORTEX. Proofs from comparative anatomy ; natural and experimental atrophy ; process of development ; irritation and excision of cortex with various results ; pathological lesions of limited ex- tent with secondary degenerations. The functions of the cortex in general are : (1) To receive impressions from the various sensory organs as conscious perceptions. (2) To associate these various simultaneous perceptions into a mental image or concept. (3) To retain these concepts as memories so that objects can be recognized or recalled. (4) To give expression to thought in action and in speech. (5) To restrain the flow of thought and to inhibit or control automatic and reflex acts. It has been established that various powers of perception, memory, and volition can be definitely assigned to various parts of the brain ; that each sense has its corresponding area in the cortex and each voluntary movement its point of departure from the cortex. It has been proven that perceptions leave behind them a phys- ical trace inseparably connected with the area in which they were originally received ; that irritation of this area produces a renewal in consciousness of the original perception as a memory, which may be so vivid as to appear real, being then a halluci- nation ; that destruction of this area causes a loss of the power of recalling the previous perception or of recognizing it when repeated. It has been proven that movements which are acquired by practice, and are therefore the result of conscious effort, are always initiated from a definite area ; that this area is insepar- ably related to movements ; since its irritation, by any cause, results in the production of forcible movements of the nature of spasms and its destruction produces a loss of the power of move- ment or paralysis of voluntary action. It has been proven that the use of language involves both the recollection of auditory and visual symbols and the initiation of impulses of speech and writing, thus calling into play not only the motor portion of the brain, destruction of which therefore 42 DISEASES OF THE NERVOUS SYSTEM. causes a loss of speech, but also the sensory portion of the brain, a lesion of which will also cause aphasia. There are certain areas upon the cortex of the brain, not necessarily coextensive with either lobes or convolutions, whose functions are accurately known. These areas are : (i) The sensori-motor area. (2) The visual area. (3) The auditory area. (4) The area of sensations of smell and of taste. (5) The speech areas. THE SENSORI-MOTOR AREA. The sensori-motor area includes the cortex of the anterior and posterior central convolutions which border the fissure of Ro- lando and the adjacent cortex in front and behind these convolu- tions. Each hemisphere controls movement on the opposite side of the body, but as the right hand is more generally used and is better trained than the left, this area is larger on the left hemi- sphere than on the right. The cortex of the posterior part of the second frontal convo- lution controls the movements of the eyes and head. Impulses starting from this area produce conjugate movement of these parts toward the opposite side. The eye district is below, the head district above. The lower third of the anterior and posterior central convolu- tions governs the movements of the face, tongue, larynx, and pharynx. The eyebrows and cheeks are controlled by the upper and forward part of this area ; the tongue and larynx by the lower and forward part ; the mouth, pharynx, and platysma by the hinder part. The middle third of the anterior and posterior central convo- lutions governs the movements of the upper extremity ; the shoulder motions being controlled in the anterior and upper part of this area; the elbow motions in its middle part and the hand and finger motions in its posterior and lower part. The upper third of the anterior and posterior central convo- lutions, including their junction in the para-central lobule, con- trols the motions of the lower extremity, the thigh, knee, foot, and toes being governed by various parts of this area from be- fore backward in the order named. The parts susceptible of the finest and most delicate move- ments, those directed by the most acute sensations, the lips, the DISEASES OF THE NERVOUS SYSTEM. 43 fingers, and the toes, lie furthest back in the motor area, chiefly in the posterior central convolution. Lesions in this convolution almost always cause some loss of tactile sensation as well as paralysis, and hence this area is thought to be the seat of tactile sensations as well as of movements, while some cases point to the localization of muscular sensations in the area just behind that of motion. The median surface of the hemisphere in front of the para- central lobule is known to be related to movements of the trunk in monkeys, but the cortex in front of the leg area on the con- vexity is the probable location of the trunk area in man. There are no sharply defined sections of the motor area to be assigned to special motions. Eacli motion, each part of a limb, has a wide general representation over the cortex and a special representation at a limited area. The areas of representation of different limbs merge into one another ; thus, in the representa- tion of the thumb we find that there is a focus, but that the thumb is represented over a great deal of the upper limb region, and that this representation diminishes in intensity gradually as we pass from the focus \ipward. This explains the fact that the excision of a small area does not totally paralyze the portion of the limb represented chiefly on that area. The adjacent areas represent to some extent that limb, and hence can govern it if need be. The motor centres govern motor acts rather than special muscles, each act involving a succession of movements of differ- ent joints by various groups of muscles. Cortical Spasm and Paralysis. Irritation in the motor area produced by any kind of disease gives rise to localized spasms or convulsions, called Jacksonian epilepsy. Destruction of the motor area gives rise to paralysis. The point of beginning of the spasm or the extent of paralysis depends on the part of the motor area diseased. Hence, from the character of either of these symptoms a conclusion can be reached as to the location of the disease. Cortical spasm or paralysis usually begins in the face or in one limb of one side and extends. The order of the progress also indicates the location of the disease, e.g., from face to arm, then to leg, or, vice versa, e.g., spasm of shoulder, arm and hand, vs. spasm of fingers, arm, and shoulder : the disease is most intense in the part first affected. Sensations of numbness precede the spasm. A cortical spasm begins locally, and usually 44 DISEASES OF THE NERVOUS SYSTEM. extends until one side of the body is affected. It is usually fol- lowed by temporary weakness. Consciousness is preserved. Cortical paralysis is monoplegic in type vs. subcortical paral- ysis, which is hemiplegic in type. A slowly advancing paralysis indicates a slowly extending destruction of tissue. Cortical paralysis is associated with increased reflexes, but there is no atrophy and no change in electric reactions. Contractures de- velop late. THE VISUAL AREA. The area of sensations of sight is located in the occipital lobe of the brain, including the cuneus on the median surface and the occipital convolutions on the convexity. The cortex lying in the calcarine fissure is the part primarily reached by the visual im- pulses, but the parts named are also concerned in vision. Each occipital lobe receives impressions from one-half of both eyes, hence a lesion in one lobe produces hemianopsia, a half-blind- ness in both eyes, the blind field of vision being on the opposite side to the lesion. This is termed homonymous hemianopsia, that is, a blindness in the like named halves of both visual fields. When the right occipital lobe is affected the patient cannot see anything on the left side of the middle line as he looks forward. Irritation of the occipital lobe may cause hallucinations of light or even of objects which are referred to the opposite visual field. Destruction of the occipital lobe on the left side destroys sight memory pictures, hence recognition of things seen may be impossible, and reading power may be lost. THE AUDITORY AREA. The area of sensations of sound is located in the first and second temporal convolutions of the brain. Each ear is connected with both hemispheres ; hence deafness from a unilateral lesion is only partial and is not generally noticed. But if both temporal lobes are destroyed the patient becomes totally deaf. Irritation of the temporal cortex may cause hallucinations of hearing. This may be the first symptom of a convulsion whose origin is an irritation in this part of the cortex. Destruction of the tem- poral cortex on the left side causes word deafness. (See speech areas.) DISEASES OF THE NERVOUS SYSTEM. 45 THE SMELL AND TASTE AREA. The area of sensations of smell and taste is located at the tip of the temporal lobe on its under and inner surface, which rests on the sphenoid bone. Each lobe is related to sensory organs on both sides, and a unilateral lesion does not often produce notice- able symptoms. THE SPEECH AREAS AND APHASIA. The speech areas are of four kinds and in four locations. They are limited to the left hemisphere in right-handed persons and to the right hemisphere in left-handed persons. There is the motor speech area in the posterior part of the third frontal convo- lution (Broca's convolution), in which the movements concerned in the act of speaking are controlled. The use of language and the power of talking are affected when this region is destroyed. There is the auditory speech area in the first and second temporal convolutions, in which the memories of word-sounds are stored up. The understanding of language and the power of recollecting the names of objects are lost when this region is destroyed. There is the visual speech area in the occipital and lower parietal region, in which the memories of printed words are stored up. The understanding of written language and the power to read are lost when this region is destroyed. The power of writing is a part of speech and is usually lost when the motor speech area is destroyed, but its exact location is not fully determined ; some cases pointing to the second frontal convolution, others to the lower parietal convolution near the hand centre as its probable cortical position. It is accepted that every word in ordinary use has a complex mental substratum, which may be termed the word-image, made up of a number of memory-pictures. The memory of the sound of a word as spoken, the memory of the appearance of the word as printed, the memory of the muscular movements needed to write the word or to pronounce it, are known to be distinct from one another and yet to be associated together. Loss of one of these memory-pictures, or disturbance in their association, im- pairs the integrity of the word-image, and produces such de- fects in its use as are indicated by the names given to the re- spective varieties of aphasia. A division of disturbances of 46 DISEASES OF THE NERVOUS SYSTEM. speech has been made into two great classes of sensory and motor aphasia the first due to defect in the receptive, and the second due to impairment of the emissive functions of the brain. A further subdivision into several varieties has been made. These are word-deafness, word-blindness, agraphia, motor apha- sia, and paraphasia. But, before considering these defects, let us look at the physical basis of the thought which lies back of the word. Take the idea " bell " as an example. The idea of a bell is made up of separate memory-pictures of its shape, size, color (visual picture) ; weight (muscular sense picture) ; cold smooth surface (touch picture) ; and sound (au- ditory picture). These various memories, received by different senses and stored up in different parts of the cortex, are asso- ciated together in a mental image of the object bell. To this mental image the word image is added of the word bell as heard, as printed, as spoken, as written, making up a con- geries of memory-pictures forming a " concept." Any one of these memory-pictures may be lost by disease. If the memories of the object are lost the symptom is called apraxia. If the memories of the word are lost the symptom is called aphasia. To examine an aphasic thoroughly it is necessary to test 1. The power to recognize objects seen, heard, felt, tasted, or smelt, and their use. This will determine whether the condition of apraxia is pres- ent. 2. The power to recall the spoken name of objects seen, heard, handled, tasted, or smelt. 3. The power to understand speech and musical tunes. 4. The power to call to mind objects named. This will test the integrity of the auditory speech area and of the association-tracts between other sensory areas and the tem- poral convolutions. 5. The power to understand printed or written words. 6. The power to read aloud and to understand what is read. 7. The power to recall objects whose names are seen. 8. The power to write spontaneously, and to write the names of objects seen, heard, etc. 9 The power to copy and to write at dictation. 10. The power to read understandingly what has been writ- ten. These tests will determine the condition of the visual word- DISEASES OF THE NERVOUS SYSTEM. 47 memories in the angular gyrus, and of the connections between this area and surrounding sensory and motor areas. 11. The power to speak voluntarily, and if it is lost, the char- acter of its defects. 12. The power of repeating words after another. This will test the integrity of Broca's centre and its associa- tion-tracts. 1. Word Deafness. If the memory of the sound of the word is lost, the word cannot be called to mind and cannot be recognized when heard. Show the patient a watch, and he is unable to name it ; tell him it is a stone, a match, a watch, and notice whether he dissents from the former and gives signs of satisfaction at the last. If he does, he has only auditory amnesia, but not word- deafness. If not, he is word-deaf, and is unable to understand what is said to him. The lesion lies in the posterior half of the first and second temporal convolution in the left hemisphere in right-handed ; in the right, in left-handed persons. This is one variety of aphasia whose lesion is well known, though it rarely occurs alone. 2. Word Blindness. If the memory of the appearance of the word is lost, the visual image of it cannot be called to mind or recognized, and then the patient will be unable to write spon- taneously, for he cannot remember how the letter looks which he wishes to write ; and he will be unable to read because the shapes of the letters and words seen arouse no recollection. As a matter of fact, words are forgotten more easily than letters, and if a patient is to relearn to read he must begin with letters and go on to words. Figures are sometimes recalled when words are forgotten, and many a patient can do mathematical calculations on paper who cannot read or write ordinary words. The reverse may also be true, the patient being able to read and write, but being unable to understand figures or calculate. Such patients may also play cards or other games, if they are not psychically blind. It is not infrequently the case that persons who are thus word-blind can write at dictation, or copy, and yet show no evi- dence of understanding what has just been read or written. A distinction must be made between those who can and cannot do these things, though its pathological basis is still obscure. The condition of visual amnesia with word blindness is due to a lesion involving the inferior parietal convolutions and angular gyrus, and is often associated with psychical blindness, but may occur inde- 48 DISEASES OF THE NERVOUS SYSTEM. pendently of it. Word-deafness and word- blindness frequently occur together, and then the lesion is found involving both the temporal and the angular convolutions. Some cases of this con- dition have depended on a deep lesion in the temporo-occipital region, breaking the association tracts. 3. Motor Aphasia. If the memory of the effort needed to pro nounce a word is lost, a true paralysis of active speech occurs, though the muscles may not be weakened. This is the ordinary form of motor aphasia, due to a lesion of Broca's centre. It is to be noted that such a loss of speech involves a loss of the power of repeating words after another, as well as of voluntary speech, and is not accompanied by any inability to understand spoken or written language. In the uneducated, as in children, the acts of talking and writing are closely joined, as may be seen by watching the lips, which move in the act of writing. But among those accustomed to write much these acts are independ ent, and it is probable that many educated aphasics may be able to answer questions in writing when their efforts at speech fail. Reading aloud will also be lost in motor aphasia, for here, too, the inability to articulate hampers the patient. 4. Agraphia. The independence of the effort-memory neces sary for writing, and connected with movements of the hand from the effort-memories of speech, has been alluded to. When these are lost alone the condition is known as agraphia. In such a state the pen cannot be used. Copying, writing at dictation, and voluntary writing are all lost. It has been noted already that when a word cannot be called to mind it, of course, cannot be written. But words can often then be written at dictation, if the person is one who writes much. Hence sensory agraphia and motor agraphia must be distinguished ; the former being a part of word-blindness, the latter not at all associated with inability to read. The lesion of motor agraphia is unsettled, though a few facts point to the posterior part of the second frontal convolu- tion as the probable seat of this function. It is not unlikely, however, that the more exact localization of fine movements of the thumb and fingers in the posterior central convolution by Horsley may be followed by the discovery of the writing centre in this vicinity. 5. Paraphasia. These forms of aphasia are due to a loss of distinct memory-pictures. The several memory-pictures which are united in the word image may thus be reasonably regarded DISEASES OF THE NERVOUS SYSTEM. 49 as separate from one another in their location in the brain. But since they are joined together to form the word-image, it follows that the association-fibres joining the various areas are as neces- sary to the use of even a single word as the various areas with their memories. It is really by association only that an object or a word becomes a subject of thought or use. If these associa- tions are broken the result is a defect of language characterized by the misplacement of words, and the patient talks jargon. There are many forms of paraphasia as there are many asso- ciation tracts, and it is not yet possible to assign different cases to their lesions. , It is evident that many differently located lesions will pro- duce disturbances of speech. When the entire cortex is dis- eased as in paresis aphasia also appears. Defects in the appreciation and use of music are called amusia, and present the same varieties as aphasia. THE FRONTAL REGION. There appears to be a certain relation between the frontal lobes of the brain and the higher forms of intellectual activity, the powers of fixing the attention and of reasoning and of self- control. But disease here does not cause a loss of any one men- tal faculty, and for the higher powers of the mind a general in- tegrity of the entire brain, not of any one part, is necessary. When it is considered that every concept is made up of numer- ous memory pictures joined together, each of which has a sepa- rate location in the brain cortex, it becomes evident that to the process of thought a healthy state of the entire cortex is neces- sary and also of the white matter beneath it, through which the associating fibres pass. And it is therefore impossible for a single lesion anywhere to cause a loss of memory or of imagina- tion or of judgment. Yet for the co-ordination of facts into or- derly series, for comparison, and for analysis of knowledge gained through the senses, the healthy state of the frontal lobes appears to be necessary. And lesions in the frontal region, especially upon the 'left side, are quite uniformly attended by mental dulness, apathy, lack of power of concentration, and im- perfect self-control. There are large areas of the cortex of the brain whose func- tion is undetermined. These are much more extensive on the 5type occur frequently in patients who may be assigned to any one of these groups. I. Infantile Hemiplegia. -The symptoms are the sudden de- velopment of a unilateral paralysis after a series of convul- sions attended by high fever and its attendant discomforts, and 62 DISEASES OF THE NERVOUS SYSTEM. a period of unconsciousness of varying duration ; then a grad- ual improvement in the paralysis after the active manifesta- tions of the onset have subsided ; and finally, a stationary condi- tion, in which the face is but slightly affected in its voluntary or automatic movements ; the speech is usually regained, if it had been lost ; the arm is quite seriously paralyzed, the fingers being stiff and awkward, and sometimes being in constant slow invol- untary motion (athetosis) ; the leg is held rather rigid, so that the child limps in walking, and often develops a club-foot. There are, of course, on the one hand, light cases in which the symptoms finally amount merely to clumsiness in the fingers. There are, on the other hand, severe cases in which a double hemiplegia has occurred, both halves of the body being equally affected, and in which both arms are useless and both legs so stiff, so closely adducted, and so helpless that walking is impos- sible (diplegin). The latter are cases in which all the symptoms date from birth. In all cases the paralyzed limbs are found to be affected in their growth and development, so that they are smaller, colder, stiffer, and weaker than the others ; the reflexes are exaggerated, but the electrical reactions are not qualitatively changed, and the sensation is normal. This condition remains through life as a permanent defect, and although the division of contractured muscles or tendons, and the application of ingen- ious apparatus, may correct deformities and make the paralyzed parts fairly useful, and although the application of electricity to the muscles chiefly affected may increase their nutrition and thus prevent contracture which comes from the unbalanced strain between the various muscles, yet any great degree of improve- ment is impossible. In more than one-half of these cases epi- leptic attacks are of frequent occurrence. The cases which date from birth must be divided into those in which there has been evidence of traumatism during labor, and those in which there was none. In the former class it may be stated confidently that cerebral hemorrhage, usually menin- geal, is the cause of the symptoms. In the latter class it is prob- ,jible that an intra-uterine encephalitis or some unknown cause ha? prevented the foetal brain from developing. ^he cases which have developed suddenly after birth are cases i n which the ordinary causes of hemiplegia in adults have been a^ng* a d must be traced either to encephalitis, hemor- rhage, P r embolism, or disease of the vessels. The degree of \ DISEASES OF THE NERVOUS SYSTEM. 63 spontaneous recovery in any case can be pretty well determined by an examination at the end of the second year. A complete cure never occurs. The fits in organic epilepsy are likely to be more frequent and severe than in idiopathic epilepsy ; as many as twenty con- vulsions may occur daily for weeks at a time. These fits do not destroy life, but render life a burden. When, however, they are infrequent they may be benefited to some degree by the use of bromides. II. The second class of cases presents mental defects more noticeable than physical symptoms. The child may be slow in learning to talk, may seem unable to fix its attention upon any- thing continuously, may be exceedingly active, in constant mo- tion the activity being, however, aimless ; may throw things about, or tear things up, or put everything into its mouth ; may be very difficult to manage because of its inability to retain and combine impressions with sufficient power to reason upon them ; and may, therefore, be incapable of appreciating the meaning of punishment, if this be inflicted. Such children may have good powers of perception, may recognize persons and objects, show pleasure at bright colors, or music, or caresses, but fail to show evidence of thought in the sense of reasoning power, judgment, or self-control. Some patients constantly drule at the mouth, cannot be taught cleanly habits, and are manifestly imbecile. Other patients are quite bright in many directions, may even be precocious, show talents in music, or drawing, or fondness for mathematics, designing, languages ; yet are apparently unable to appreciate moral ideas, cannot be taught to tell the truth, are cruel and bad, will not control any of their impulses, and so are the distress and despair of parents and teachers. It is those men- tal qualities which are the product of the highest evolution which have failed to develop in this class of cases. The final result is that they have to be taken care of all their lives, either at home or by attendants, being incapable of supporting themselves or directing their conduct. Many of them have epilepsy. Some of them have hemiplegia. III. The third class of cases is less common than the two preceding, and is likely to escape observation unless carefully investigated. The patients belonging to this class may be hemi- plegic or may present no motor or mental defects, though they may be the subjects of epilepsy. They do have defects of sen- 64 DISEASES OF THE NERVOUS SYSTEM. sory perception. Such defect may be in the form of hemianopsia or of deafness. It is probable that many cases of deafmutism belong to this class, and in some persons, as in Laura Bridgeman, deafness, dumbness, and blindness coincide. The pathological changes in the brain in these various cases dif- fer widely, and are as follows, in the order of frequency : Porencephalus, a localized atrophy or agenesis, leaving a cav- ity in the cerebral hemisphere, which may be deep enough to open into the ventricle. Sclerotic atrophy, an atrophic condition of the brain with an increase of connective tissue and disappearance of the nervous elements ; affecting both hemispheres, or one only, or a part of one only ; or limited to small areas in various parts. Maldevelopment and apparent atrophic condition of the minute structures of the hemisphere, chiefly cortical, the cells resembling those of a new-born child, but with no apparent gross defects in the brain. Atrophy, consequent upon the condition of softening pro- duced by embolism or thrombosis, and limited in extent to cer- tain arterial districts of the brain. Meningo-encephalitis, a condition shown by thickening and ad- hesion between the pia and the brain, with destruction of the cerebral cells and atrophy of the cortex. Cysts lying on the brain and producing atrophy by pressure, or associated with atrophy due to the original lesion of which the cyst remains as a trace. Hemorrhage on, or in, the brain, as shown by the remains of a clot, or by hematin staining of a cyst, of the pia, or of the scle- rotic tissue. Hydrocephalus with extreme dilatation of the ventricles, so that the brain-tissue is reduced to a mere wall about the cavity. These are the conditions found at death in cases presenting the clinical features just studied. It is evident that they have this in common, namely, a condition of atrophy of the brain. The origin of this atrophy is not always clear. In some cases it is clearly congenital and due to a maldevelopment of the em- bryo. In other cases it is clearly traceable to injuries at birth. In other cases it must be ascribed to affections of various kinds, such as inflammations of the membranes, or of the brain sub- stance, or vascular lesions and their consequences, such as occur in adults. But it is evident that the various processes of disease DISEASES OF THE NERVOUS SYSTEM. 65 have as a fairly uniform result a condition of atrophy with scle- rosis of the brain, which may be termed sclerotic atrophy. The difference in the clinical types is due to the varying situation of the lesion rather than to its varying nature. For such conditions there can be no treatment. TUMORS OF THE BRAIN. Varieties in order of frequency : Gumma : soft gelatinous, or hard cellular, situated on base or in cortex, usually beginning in meninges. Tubercular: hard masses, often multiple, especially frequent in children, situated anywhere, sometimes primary, usually sec- ondary. This is the variety in more than one-half the cases in children. Glioma : peculiar to the nervous system, cells and fibres like the neuroglia, usually infiltrated and without boundaries, but single, usually vascular, hence symptoms vary and hemorrhage occurs ; usually situated in the white substance. Sarcoma of all varieties : fibro-, round-cell, spindle-cell, glio- sarcoma, begin from connective tissue of membranes as a rule, sometimes in the brain. Hard single tumors, of various sizes, easily separable and well defined, situated on base, in meninges, in cerebellum. Carcinoma : rare, usually secondary. Occasional varieties are fibromata, osteomata, psammomata, cholesteatomata, angiomata, lipomata, r echinococcus, and cysti- cercus. Aneurisms of the base give rise to symptoms of tumor. For Pathology of Tumors see Delafield and Prudden's " Pathology." Causes of Brain Tumor. i. Predisposing : Sex : males twice as frequently affected as females. Age : children most liable, as tubercular tumors are frequent. Young adults next. Old age is quite exempt, except from carcinoma. 2. Exciting. Injuries. Severe emotional shock. Unknown in large majority. Situation. Cerebral cortex, twenty-five per cent; cerebel- lum, twenty-five per cent.; centrum ovale, fifteen per cent.; basal ganglia, ten per cent.; pons, ten per cent.; crus and corpora quadrigemina, ten per cent. Others five per cent. 66 DISEASES OF THE NERVOUS SYSTEM. Effects of Brain Tumor. i. Direct effects, irritation of gray matter with nervous discharges ; and destruction of brain tissue. 2. Indirect effects. General pressure on entire brain. This may be limited by the falx or tentorium. It produces hydro- cephalus by pressure on ventricle or veins of Galen. Vascular disturbance by pressure on arteries and veins. Meningitis, local- ized and not purulent except in tubercular cases. Thinning of cranial bones. Effects of increased pressure are seen after death in flatten- ing of the convolutions, anaemia and pallor of the brain, dry sticky state of membranes and distention of ventricles by serum. Symptoms of Brain Tumor. I. General symptoms depend on existence of a new growth independent of its position. Headache in ninety-five per cent., constant or intermittent : general or local ; dull and deep, increased by anything which deranges the cerebral circulation. Sometimes head is tender to percussion at certain points : may have evidence of pain even in state of stupor : it may be agonizing ; it may give feeling of band about head : it is often worse at night, causing insomnia, especially in gumma. Mental disturbance, eighty-five per cent. Dulness and apathy, with imperfect attention and memory. Depression and emo- tional state. Slow speech, gradual mental failure, childishness 1 and dementia ; fainting attacks, stupor and coma in the last stage. Occasionally delirium and active insanity. Optic neuritis, eighty per cent. Venous congestion. Swell- ing of papilla, loss of disc outline ; radiating appearance about the disc and hemorrhages ; then optic nerve atrophy leaving white or gray disc. In cases of subcortical tumor of small size it may be absent. Sight may be affected ; visual field small and irregular, or unimpaired for a time. Vertigo or sense of giddiness, frequent in tumors in posterior fossa. May occur in tumors anywhere on change of position. May be due to paralysis of one or more ocular muscles. Vomiting, with or without nausea or relation to food. Fre- quent in tumors in posterior fossa. General convulsions of epileptic type. Petit mal vv grand mal. Nystagmus, lateral oscillation of eyes. Frequent in disease of corpora quadrigemina and cerebellum. Loss of control over sphincters occurs, especially with tumors in the frontal lobes. DISEASES OF THE NERVOUS SYSTEM. 67 Glycosuria and polyurea, especially with tumors in the pos- terior fossa. Slow pulse ; 50 to 60. II. Local Symptoms dependent upon the position of the tumor. Frontal Lobes: Mental dulness, lack of control of emotions, irritability, inattention, and childishness, dementia, loss of sense of smell. Left third frontal convolution. Motor aphasia. Central Convolutions, and motor tract. Monospasm and mono- plegia when in or near cortex. Hemispasm and hemiplegia, when deep or in capsule. Sometimes slight anaesthesia in par- alyzed part. Occipital Lobe and visual tract. Hemianopsia, noticed by pa- tient as unilateral blindness. Visual hallucinations and flashes of light on one side. Left Temporal fast and second convolutions. Sensory aphasia : form, word-deafness. Left Lower Parietal lobule and angular gyrus or in occipito- temporal tract. Sensory aphasia : form, word-blindness. Base of brain. Anterior fossa : Loss of smell. Middle fossa: Hemianopsia, paralysis of ocular muscles, III., IV., VI.; neuralgia of face and anaesthesia, V.; paralysis of III. and opposite hemiplegia, neuroparalytic ophthalmia, nystagmus ; bilaterial spastic paralysis, deafness. Posterior fossa : Paralysis of VII., IX., X., XL, XII.; vertigo and aural symptoms; cerebellar ataxia, tendency to one side; paralysis wide-spread from medulla disease. Cerebellum : Vertigo, vomiting, cerebellar ataxia when mid- dle lobe is involved ; headache, frontal or occipital and severe ; optic neuritis early. Diagnosis. Cerebral symptoms : general alone, or general + local, point to the presence of a tumor. Differentiation from chronic nephritis : By examination of urine ; by condition of heart, arteries, and blood-pressure ; by appearance of optic disc and retina in many cases, haemorrhages more frequent and white spots far from disc ; by character of headache, more severe in tumor ; by age of patient, young per- son = tumor. From hypermetropia with astigmatism and anaemia, with 68 DISEASES OF THE NERVOUS SYSTEM. menstrual disorder : By examination of eyes and relief of glasses ; by cure of anaemia by diet, iron, and aloes ; by slight degree of headache and neuritis. From hysteria with migraine : By study of the patient and separation of real symptoms ; by condition of the optic disc. From abscess : By history of trauma or of otitis media ; by severity of early symptoms in abscess ; by fever in abscess ; by late development of optic neuritis, rare in abscess. To determine the location : Study carefully the local symp- toms, " signal symptom," e.g., numbness and twitching of thumb. Study also the order of appearance of local symptoms : thumb, hand, face. Compare the several local symptoms, paralysis + aphasia, or + hemianopsia. To determine the variety : Estimate probable frequency of various tumors at different ages. Look for history of syphilis, tuberculosis, cancer, or sarcoma. Study rapidity of onset ; gli- oma, tubercle, cancer are rapid. Study signs of irritation ; more frequent in glioma and meningeal tumors. Study signs of varia- tion in severity of symptoms ; more variation in glioma. Study situation of the tumor ; basal tumors are often gum ma, tubercle sarcoma. Intra-cerebral tumors are often glioma, sarcoma. Pe- culiar forms of hemiopia and early optic neuritis indicate sar- coma of pituitary body or aneurism. Course of the disease : Begins with general symptoms usually. Sometimes begins with local spasm or a general convulsion. Gradual increase in severity and number of symptoms. Finally death in stupor or in general convulsion or suddenly, from heart failure, or recovery under specific treatment. Duration is from one to three years. Prognosis bad excepting in gumma and when tumor can be removed. Treatment. For gumma : Inunctions of mercury and KI to three hundred grains daily. Surgical treatment : Removal is possible when diagnosis of location is exact. There is danger of return. For Cranio-Cerebral Topography, see page 40. ABSCESS IN THE BRAIN. Acute encephalitis with formation of pus results in an ab- scess. The abscess may extend rapidly, not being encapsulated, DISEASES OF THE NERVOUS SYSTEM. 69 and cause death ; or it may become encapsulated and develop slowly, or become stationary and remain for years as a foreign substance producing no symptoms, but finally enlarge or break. Occasionally multiple abscesses develop in the brain secondary to pyaemia, producing cerebral symptoms in the course of that disease. There may be a secondary meningitis in either form. Situation. Is usually in the temporo-sphenoid lobe or in the frontal lobe or in the cerebellum, in the white matter. Causes. Chronic otitis media, forty per cent. Fracture of cranial bones, thirty-five per cent. Chronic rhinitis, ten per cent. Caries of any cranial bone, ten per cent. Secondary to infectious diseases, five per cent. Symptoms. After an injury or after otorrhoea or other cause cerebral symptoms develop suddenly ; severe headache, vomit- ing, mental distress and dulness, stupor, a chill, a high tempera- ture for a day or two ; possibly convulsions ; rarely local symp- toms ; hemiplegia, hemianopsia, aphasia, cerebellar staggering. In a week the patient is very ill, with irregular temperature, sometimes with chills, sometimes no fever ; slow pulse ; intense pain, delirium, stupor, and optic neuritis. If abscess extends death follows in two weeks, or suddenly from rupture. If ab- scess discharges into ear or nose, or if it can be opened, symp- toms subside. Rarely symptoms subside spontaneously slowly, the abscess becoming encapsulated and latent, and patient ap- parently recovers, but is subject to headache and vertigo ; and has a relapse later. Diagnosis. ABSCESS Temperature normal or not high. Pulse slow. Patient in stupor. Spasms and rigidity rare. Cranial nerves not involved. Optic neuritis frequent. ABSCESS Temperature normal or not high. Pulse slow. Chill at onset not repeated. Little sweating. Head tender to percussion ? vs. MENINGITIS. Temperature high without remission. Pulse rapid. Patient irritable, all senses over acute. Spasms and rigidity frequent. Cranial nerves involved early. Optic neuritis rare. vs. THROMBOSIS OF LATERAL SINUS. Temperature high with remissions. Pulse rapid, weak. Chills frequently repeated. Profuse sweating. Pain over mastoid and jugular. , Thrombi in lungs. 7O DISEASES OF THE NERVOUS SYSTEM. Diagnosis of location is made partly from the exciting cause and partly from the local symptoms. Prognosis fatal, unless abscess can be opened. Treatment. In the few cases in which the abscess can be located operation of trephining and drainage. CEREBRO-SPINAL SCLEROSIS. Multiple or disseminated sclerosis is a rare disease affecting the brain and spinal cord together. Small regions of sclerotic tissue are found irregularly scattered through the entire nervous system, without destruction of the axis cylinders of the nerve tracts. Its cause is unknown. Symptoms. Headache, vertigo, malaise, mental irritability, inattention, imperfect memory, lack of self-control, and inability to work. Later tremor of hands increased by an effort to hold them still, nystagmus, increased knee-jerk, stiff spastic gait, weakness, and finally general tremor on effort. Slow speech, each syllable separately enunciated without variation of tone. Optic atrophy. Dementia and attacks of epilepsy and hemi- plegia may finally occur. Course is exceedingly irregular, symptoms may disappear for months and then return. The disease is often mistaken for hysteria. Diagnosis is made by excluding all other organic diseases, by nystagmus, tremor, and speech. Treatment. Physostigmine, Jg- gr. daily ; solanin, | gr. daily, increased. FUNCTIONAL NERVOUS DISEASES. NEURASTHENIA. Nervous prostration, nerve tire, nervous irritable weakness is a functional disease of the entire nervous system, brain, spinal cord, spinal and sympathetic nerves, dependent upon malnutri- tion, characterized by nervous weakness and irritability. A balance between expenditure of energy and nutrition must be preserved. Brain over-work or anxiety ; Spinal cord over-work by long marches or sexual over-action ; Nerve over-work by various occupations in which a single act is repeated ; Vaso-motor work in maintaining vascular tone and nutritive processes, all require a sound basis and rest at periods. When balance between store and expenditure of energy is broken, exhaustion results. Then nature enforces rest by fa- tigue, by sleep. One may disregard nature, but if so one must pay the penalty. Causes. I. Excessive expenditure of nerve energy. Primary neurasthenia more common than secondary. Influences favoring its production : 1. Bad hereditary influences. Weak nervous system. 2. Feebleness in childhood, with poor nervous system. 3. Wrong methods of training and education. 4. The struggle for existence. Kant's rule, eight hours for Avork, eight hours for diversion, eight hours for sleep. 5. Anxiety, worry, mental depression, fear. 6. Mental or physical over-work. 7. Sexual excesses. II. Deficient supply of nervous energy. Secondary neurasthensia. Influences favoring its production. i. Weakening diseases of all kinds of organic nature. 72 DISEASES OF THE NERVOUS SYSTEM. 2. Indigestion and dyspepsia, with auto-infection by products. 3. Gout, rheumatism, uric-acid diathesis. 4. Infectious diseases, typhoid, grippe, malaria. 5. Alcoholism or abuse of drugs. Result of the action of these causes is to produce malnutri- tion of the nervous system and state of irritable weakness. 1. The power of continuous activity is impaired ; weakness results ; hence, mental work is imperfect ; attention flags ; mem- ory fails ; ambition ceases ; physical activity is imperfect ; ex- ercise tires one ; lassitude ; vegetative functions are impaired. Digestion is poor; constipation occurs; vascular tone is im- paired ; heart feeble. Balance must be maintained between blood supply and functional activity. When this is impaired work is impossible. Secretions are changed in amount and character, e.g., urine. 2. The power of mental and physical control is impaired and irritability results ; inhibition may be partly automatic and partly conscious ; it must be conscious and voluntary to prevent mor- bid fear and apprehension ; influence of fear is to inhibit all ner- vous acts e.g., walking on ice, oral examination, stage fright ; this control is weakened, and hence irritability results. Symptoms of Neurasthenia. 1. Cerebral : Headache dull, occipital, frontal ; sensitiveness of scalp ; vertigo ; insomnia ; cerebral sensations fulness, band, pulsation. 2. Mental : Apprehension morbid fears, of places, people, solitude, etc.; inattention and forgetfulness ; incapacity for work ; idiosyncrasies become prominent ; irritability of temper ensues ; anxiety and exhaustion ; imperfect respiration and rapid pulse. 3. Spinal : Pain, especially in nape of neck and sacrum ; irri- tation ; hypersensitiveness ; sensitiveness about ribs and inter- costal nerves ; weakness, legs give out ; sexual irritation, erec- tions, impaired power ; emissions ; bladder irritability, frequent micturition. 4. Vaso-motor : Flushes, cold extremities ; undue sweating ; transient blueness or oedema ; tac/ie cerebrale of Trousseau ; tachy- cardia ; palpitation. 5. Gastro - intestinal : Indigestion and dyspepsia, especially acid stomach ; imperfect liver action ; constipation ; pseudomem- branous colitis ; distention of abdomen with gas. DISEASES OF THE NERVOUS SYSTEM. 73 6. Sensory and motor symptoms: Indefinite pains and paraes- thesia ; joint affections ; apparent paralysis no change in elec- tric activity ; vision imperfect ; asthenopia ; visual field may be retracted. Other senses rarely affected; tinnitus. Diagnosis made by the existence of a cause ; the absence of objective signs of organic disease ; the temperament of the pa- tient ; the variability of symptoms ; the disproportion between complaint and actual power. Treatment. Absolute necessity of establishing nerve-energy by restoring balance between store and expenditure. Hence sup- pi v nutritive elements to nervous system by proper food, prop- erly digested ; by increasing circulatory power ; by exercise ; by hydrotherapy ; by massage ; and diminish expenditure of nervous energy by rest, if necessary absolute, and by diversion. Direct treatment may be by tonics of all kinds ; by sedatives, if patient is extremely nervous ; by electricity ; galvanism. Treat symptoms only when absolutely necessary. Combat the desire of these patients for drugs, and their dependence on stimu- lants and opiates. HYSTERIA. A functional disturbance of the nervous system characterized by mental and moral perversion, lack of self-control and disor- ders of any or all of the bodily functions. Women, between fifteen and twenty-five years, or at any age. Men, at any age, and even children, may be affected. Causes. Hereditary influence very marked ; malnutrition of the nervous system from anaemia ; indigestion ; from bad habits of life ; emotional excitement ; fear, anxiety, jealousy ; tendency to imitation yielded to ; epidemics of hysteria ; uterine and ova- rian irritation is a rare cause. Traumatism, especially accidents attended by great fear. Several causes may concur. Symptoms, i. Mental changes, and moral perversion. Increased irritability, and emotional excitability with impaired self-control. Excessive emotion leads to exhaustion. Craving for notice and sympathy. All sorts of means taken. Self-injury; sores which won't heal ; needles swallowed ; blood sucked and vomited ; animals concealed. Purposeless acts of criminal kind, like reasoning mania. 74 DISEASES OF THE NERVOUS SYSTEM. Hallucinations may occur. Depression is not uncommon, and melancholia may be feared. But in melancholia facial expression is characteristic, thought is slow, delusions are of self-accusation, weight is rapidly lost. 2. Disorders of various functions : (1) Motor. Spasms, contractures, paralysis, convulsions, glo- bus hystericus, vomiting, diarrhoea, vesical irritation, convulsion attended by sobbing and crying, lasts longer than an epileptic- fit, does not begin or end suddenly, and tongue is not bitten, and there is no asphyxia. Paralysis, varies in intensity, does not af- fect the face in hemiplegia, no typical gait, no bed-sore, no in- continence ; aphonia, aphasia, cough. (2) Sensory. Hyperaesthesia of special senses, dislike of light or noises ; hyperaesthesia of skin, spinal irritation ; hyperaesthe- sia of limbs, numbness ; hyperaesthesia of ribs, pressure of dress ; hyperaesthesia of ovaries ; hyperaesthesia of bladder, frequent micturition ; pain anywhere, rarely definitely localized ; especially in joints, hip, knee, ankle, wrist, elbow ; fixation, atrophy of mus- cles ; joints easily moved under ether ; no deformity ; anaesthe- sia to pain, usually localized, in skin or mucous membranes ; uni- lateral loss of special senses. (3) Vaso-motor. Palpitation and faints ; variations of arterial tone, flashes, oedema ; hematemesis, haemoptysis ; small hemor- rhagic spots, stigmata ; rises of temperature, 105 to 110 F. (4) Secretion. Saliva ; gastric juice varies. Urine or +. Hysterical attacks : Crying and laughing, produced by emo- tional strain ; scream, convulsion, opisthotonus, facial expression, series of short attacks, fit of crying, passes water, cataleptic rigidity, hystero-epilepsy. The character of the symptoms varies greatly. The symptoms appear and disappear suddenly. The course of the disease : Chronic condition with periods of intensity ; cure, sudden and marvellous ; great variation in symptoms ; very rarely death in convulsion or from suicide. Diagnosis is never made from a single symptom but from a study of the general condition. Treatment. Mental change and moral education ; hydrother- apy ; the rest cure ; mental therapeutics ; tonics, strychnine, iron and quinine. Symptomatic remedies : DISEASES OF THE NERVOUS SYSTEM. 75 Sedatives for the nervous state, bromides, valerian, lavender, asafoetida. Opium is to be avoided, for habit is easily formed. For convulsion, prevent injury, don't use chloroform, use cold water, hold patient, stop respiration, don't press ovaries, give emetic. For faints, irritation over heart by ice, internally spirits am- monia, or lavender. For spasms, hot or cold applications, cautery. For paralysis, electricity, especially faradism. For pain, hypodermics of water after one of morphine, local applications of sedatives. 1. Normal Nerve Fibre, a, Axis cylinder; 6, medullary sheath; c, sheath of Kchwann; d, node of Ranvw e, incisure of Schmidt; /, nucleus of sheath of Scliwann. - "~ " Fra. '<}. -Degeneration of Nerve Fibres in Various Stages. FIG. 3. -Cross Section of Normal and Degenerated Nerve Trunk. 1 I C Fio. 4. The Spinal Cord with its Nerves (Anterior Sur- ;e). Brachial, Lumbar, and Sacral Plexuses and Nerves Extremities shown on left: Sympathetic Ganglia with Spi- 1 Roots shown on right of the figure. FIG. 5. The Relation of the Spinal Con the Vertebral Bodies and Spines. The ends at L. I. FIG. 6. Diagram of a Spinal Segment as a Spinal Centre and as a Conducting Medium (Bramwell). B, Right; B', left hemisphere ; MO, medulla oblongata ; 1, motor tract from right hemisphere; at MO it divides into a direct and a crossed tract, the former passes down the right ant. median column, the latter passes down the left lateral column, giving off at 1' fibres to the ant. gray horns of the cord, in which the motor cells lie, from which nerves pass to muscles, M; 2, motor tract from left hemisphere; S, S', sensitive areas on the left side of the body; 3. 3', the main sensory tract from the left side of the body; it passes into the post, gray matter of the segment, then decussates, and passes up the right half of the cord in the post, columns, thence to the right hemisphere of the brain; 4, 4', the main sensory tract from the right side of the body; 5, 6, the tracts of muscular sense from the legs, passing up upon the same side of the spinal cord in which it enters, in the column of Goll, decussating at the medulla, above the motor decussation. The arrows indicate the direc- tion of nerve currents. Fio. 7. Diagram of a Section of the Spinal Cord in the Cervical Region. A.C., Ant. commissure; P.O., )st. commissure; I.g.s., intermediate gray substance; P.Cor., post, comu; c.c.p., caput cornu post. ; L.L.L., teral limiting layer; AL-AT., antero-lateral ascending tract. 3 C. II. D. VIII. C. V. D. XII. C. VII. I,. II. D. I. L. IV. S. I. FIG. 8. Sections of Spinal Cord. 1 to 6, Groups of cells in ant. horns. I.-IX.. Columns of cord. I., Ant. median. //., Anterior. III., Antero-lateral. TV.; Lateral pyramidal. V.. Lateral limiting: layer. VI., Pos- tero-lateral or Burdach. VII., Postero-median or Goll. VIII., Ant.-lateral ascending. IX., Direct cere- bellar. Between IV. and VI., Col. of Lassauer. liv FIG. 9. The Base of the Brain and the Cranial Nerves. ra, Pons and Medulla (Allen Thompson). I. to XII., The aial nerves; Th, optic thalamus; h, pituitary body; tc, 3r cinerium; a, corpora albicantia; P, pes pedunculi; i, rior, and e, exterior, geniculate body; PV, pons Varolii; anterior pyramid of medulla; o, olive; d, decussation of erior pyramids; ca, anterior column of spinal cord; cJ, ral column of spinal cord; Ce, cerebellum: fl, flocculus of sbellum. FIG. 10. Side View of Pons and Medulla to show Nuclei and Roots of Cranial Nerves. V.- XII. , nuclei ; KV.-VII.. roots of nerves; V, long ascending- nucleus of V. ; O, olive;Os, supe- rior olivary body; Gf, knee of facial nerve root. FIG. 11. The Motor Tract in the Cms, Pons, and Medulla. A, Lesion causes hemiplegia. B, Lesion causes alternating paralysis; left facial, right extremities. C, Lesion causes paralysis of limbs and tongue. D, Lesion causes paralysis of limbs of opposite side. E, Lesion in motor decussation causes bilateral paralysis. FIG. 12. The Sensory Tract in the Crus, Pons and Medulla, showing Nucleus and Roots of V Nerve. A, Lesion causes hemianaesthesia. B, Le sion causes alternating hemianaesthesia; left fa and right side of body. YL FIG. 13. Sagittal Section through the Cerebral Axis to show the Nuclei of the Ocular Nerves in the Floor of the Aqueduct of Sylvius and Fourth Ventricle and the Course of the Nerves to their Exit. The various groups of cells from which the III. N arises are seen. RN, Red nucleus of tegmentum ; L, lemniscus (sensory tract) ; CC, motor tract in the cms cerebri seen to traverse the pons and enter the ant. pyramid of tbe medulla. FIQ. 14. The Lateral Surface of the Left Hemisphere (Eberstaller). S, Fissure of Sylvius; C, fissure of Rolando, or central fissure; pel, sulcus prse-centralis inferior; pcs, "sulcus praecentralis superior; r(c, ^sulcus retro-centralis; sfr, sulcus sub-frontalis; fl,f2, /3, sulcus frontalis, sup., inf. et medius; ip, interparietal ^fls- sure; po, parieto-occipital fissure; occ. ant., occ. lat., fissure, occipitalis, ant. et lat. ; tl, to, t'i, sulci^temporales; A, B, ant. and post, central convolutions; -Pi, F, Ft, frontal convolutions, sup., med., inf.; PI, P2,~parietal convolutions, sup. and inf.; G. spm, gyrus supra-marginalis; G. ang, gyrus angularis; 0, occipital lobe; 21, T2, TS, temporal convolutions. FIG. 15. The Functional Areas of the Brain, Left Hemisphere. ,XP FIG. 16. The Median Surface of the Right Hemisphere (after Ecker). The visual centre is in the cortex lying k within[the calcarine fissure, OC, and in the cuneus, Oz. The sensations of smell and taste are received in the uncinate convolution, V, and at the tip o'f the temporo-sphenoidal lobe. A, B shows the posi- tion of the'paracentral lobule, which is included in the motor area of the leg. FIG. 17. The Association Fibres. A, Between adjacent convolutions; B, between frontal and occipital areas; C, between frontal and temporal areas, cingulum; D, between frontal and temporal areas, fasciculus uncinatus ; E, between occipital and temporal areas, fasciculus longitudinalis inferior; CN, caudate nucleus; OT, optic thalamus. FIG. 18. The Projection Tracts joining the Cortex with Lower Nerve Centres. Sagittal section showing the arrangement of tracts in the internal capsule. A, Tract from the frontal lobe to the pons, thence to the cerebellar hemisphere of the opposite side; B, motor tract from the central convolutions to the facial nucleus in the pons and to the spinal cord; its decussation is indicated at K; C, sensory tract from posterior columns of the cord, through the posterior part of the medulla, pons, crus, and capsule to the parietal lobe ; D, visual tract from the optic thalamus (OT) to the occipital lobe; E, auditory tract from the inter-geniculate body, to which a tract passes from the VIII. N. nucleus (J) to the temporal lobe; F, superior cerebellar peduncle; G, middle cerebellar peduncle; H, inferior cerebellar peduncle; CN, caudate nucleus; CQ, corpora quadrige- mina ; Vt, fourth ventricle. The numerals refer to the cranial nerves. FIG. 19. Horizontal Section through Right Hemisphere showing the Internal Capsule and Basal Ganglia. F, Fornix; NO, caudate nucleus; OT, optic thalamus: NL, lenticular nucleus; IR, island of Reil; EC, external capsule; V, lateral ventricle; 1C, int. capsule, ant. part; Fa, facial tract; M, motor tract to limbs; S. sensory tract: O, visual tract, all in the post, part of the capsule. Fio. 20. The Motor Tract. S, Fissure of {Sylvius; NL, lenticular nucleus; OT, optic thalamus; NO, cau- date nucleus; C, eras; P, pons; M, medulla; O, olivary body. The tracts for face, arm, and leg gather from the lower, middle and upper thirds of the motor area, pass into the capsule and through the crus and pons, where the face fibres cross to the opposite VII. N. nucleus, while the others pass on to the lower medulla, where they partially decussate to enter the lateral column of the cord, the non-decussating fibres passing into the ant. median columns. Lesion in cortex causes monoplegia ; in capsule, hemi plegia ; in pons, alternating paralysis. 10 & FIG. 21. The Visual Tract. The result of a lesion anywhere between the chiasm and the cuneus is to produce homonymous hemianopsia. H, Lesion at chiasm causing bilateral temporal hemianopsia; N, lesion at chiasm causing unilateral nasal hemianopsia; T, lesion at chiasm causing unilateral temporal hemianop- sia; SN, substantia nigra of cms; L, lemniscus in crus; RN, red nucleus; 1/7. third nerves. FIG. 22. Diagram to illustrate the Concept "Bell" and to show the Varieties of Apraxia and Aphasia. The memory pictures are relics of past perceptions received through different senses. The association makes up the mental image bell. The word image is made up of the memories of the sound and appearance of the word, and of the uttering and writing effort memories; these are joined together. The mental image and the word image are also joined with one another, making up the con- cept "bell." GfabfHa FIG. 23. Diagram to show the Relation of the Skull and its Sutures to the Fissures of Rolando and Sylvius. 12 FIG. 24. Photograph of Model of Head, showing Relation of Cranial Sutures to the Convolutions of the brain. R, Fissure of Rolando; J, inter parietal fissure; PO, parieto-occipital fissure; S, fissure of Sylvius: F. frontal; P, parietal: O, occipital: T. temporal lobes; A, ant. cent., and P. post. cent, convolution. fr, UNIVERSITY OF CALIFORNIA LIBRARY Los Angeles This book is DUE on the last date stamped below. Form L9-30m-7,'56(C824s4)444 tKVA. 3 1158 00346 6355